rowid,run.accession,experiment.accession,sample.accession,study.accession,bioproject,study.title,study.alias,study.type,study.abstract,study.attributes,study.PMIDs,sample.description,sample.title,sample.alias,sample.centername,sample.attributes,GEOsample.title,GEOsample.dataprocessing,GEOsample.source,GEOsample.treatmentprotocol,GEOsample.extractprotocol,GEOsample.growthprotocol,GEOsample.characteristics,GEOsample.accession,experiment.title,experiment.alias,experiment.library_name,experiment.design_description,experiment.library_construction_protocol,experiment.attributes,experiment.library_strategy,experiment.library_source,experiment.library_selection,experiment.library_layout,experiment.platform,experiment.instrument_model,experiment.spot_descriptor,experiment.study_ref,run.title,run.attributes,run.filename,run.semantic_name,run.total_bases,run.total_spots,run.alias,run.read_lengths,run.base_counts,run.r1_length,run.r2_length,run.r3_length,run.r4_length,run.Acount,run.Ccount,run.Gcount,run.Tcount,run.Ncount,run.experiment,run.pool_member,submission.accession,submission.srasource,submission.bioprojectsource,seqdetective.n_mates,seqdetective.mapping_rate.mate1,seqdetective.mapping_rate.mate2,seqdetective.nofeature_rate.mate1,seqdetective.nofeature_rate.mate2,seqdetective.sparsity.mate1,seqdetective.sparsity.mate2,seqdetective.pos_strand_rate.mate1,seqdetective.pos_strand_rate.mate2,seqdetective.readlen.mate1,seqdetective.readlen.mate2,seqdetective.judgement.mate1,seqdetective.judgement.mate2,seqdetective.judgement.reason,platform_family,instrument_generation,read_bias,selection_class,prep_kit,sc_or_bulk,tech_class,technology,tech_variant,submission.bioprojectsource.country,earliest_date,devstage_curation,devstage_curation_coarse,tissue_curation,tissue_curation_coarse
32037,SRR28992909,SRX24520261,SRS21267950,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Wt1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Wt1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Wt1,Kcnd2 Wt1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Kcnd2_Wt1.fq.gz,fastq,3386455050.0,22576367.0,Kcnd2 Wt1.fq.gz,0:150,A:967137430;C:730108913;G:738646978;T:950549427;N:12302,150,,,,967137430,730108913,738646978,950549427,12302,SRX24520261,SRS21267950,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32038,SRR28992910,SRX24520260,SRS21267949,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Hom3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Hom3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Hom3,Arfgef1 Hom3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Arfgef1_Hom3.fq.gz,fastq,3647365500.0,24315770.0,Arfgef1 Hom3.fq.gz,0:150,A:923919033;C:903440333;G:911845870;T:908147370;N:12894,150,,,,923919033,903440333,911845870,908147370,12894,SRX24520260,SRS21267949,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32039,SRR28992915,SRX24520258,SRS21267947,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Hom1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Hom1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Hom1,Arfgef1 Hom1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Arfgef1_Hom1.fq.gz,fastq,3388869300.0,22592462.0,Arfgef1 Hom1.fq.gz,0:150,A:869162615;C:827706442;G:835453288;T:856534517;N:12438,150,,,,869162615,827706442,835453288,856534517,12438,SRX24520258,SRS21267947,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32040,SRR28992912,SRX24520257,SRS21267946,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Het3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Het3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Het3,Arfgef1 Het3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Arfgef1_Het3.fq.gz,fastq,3369996750.0,22466645.0,Arfgef1 Het3.fq.gz,0:150,A:861941573;C:824864964;G:833793356;T:849388791;N:8066,150,,,,861941573,824864964,833793356,849388791,8066,SRX24520257,SRS21267946,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32041,SRR28992913,SRX24520256,SRS21267945,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Het2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Het2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Het2,Arfgef1 Het2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Arfgef1_Het2.fq.gz,fastq,4755406500.0,31702710.0,Arfgef1 Het2.fq.gz,0:150,A:1254995507;C:1127923454;G:1138127034;T:1234180808;N:179697,150,,,,1254995507,1127923454,1138127034,1234180808,179697,SRX24520256,SRS21267945,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32042,SRR28992916,SRX24520254,SRS21267943,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Hom3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Hom3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Hom3,Wnt8b Hom3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Wnt8b_Hom3.fq.gz,fastq,5283928950.0,35226193.0,Wnt8b Hom3.fq.gz,0:150,A:1389228037;C:1262004726;G:1265392219;T:1367105548;N:198420,150,,,,1389228037,1262004726,1265392219,1367105548,198420,SRX24520254,SRS21267943,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32043,SRR28992919,SRX24520251,SRS21267940,SRP506997,PRJNA1110229,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1110229,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 81 were determined suitable for the generation of loss of function zebrafish models via CRISPR/Cas9 gene editing. Of those 81 crispants  48 were successfully established as stable mutant lines and assessed for seizure like swim patterns in a primary F2 screen. Evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b of the 48 mutant lines assessed. Further characterization of those 5 lines provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Furthermore  RNAseq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Het3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Het3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Het3,Wnt8b Het3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina NovaSeq 6000,,SRP506997,,,Wnt8b_Het3.fq.gz,fastq,4357330950.0,29048873.0,Wnt8b Het3.fq.gz,0:150,A:1179652667;C:1002955689;G:1008147493;T:1166494534;N:80567,150,,,,1179652667,1002955689,1008147493,1166494534,80567,SRX24520251,SRS21267940,SRA1863814,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,,usable mapping rate,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-10,Larval,Larval,Head,Nervous System
32068,SRR29007557,SRX24534635,SRS21280318,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Wt 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Wt1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Wt 1,Kcnd2 Wt 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Wt_1_1.fq.gz Kcnd2_Wt_1_2.fq.gz,fastq fastq,6772910100.0,22576367.0,Kcnd2 Wt 1 1.fq.gz,0:150 1:150,A:1933789152;C:1464135438;G:1474439143;T:1900463092;N:83275,150,150,,,1933789152,1464135438,1474439143,1900463092,83275,SRX24534635,SRS21280318,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32069,SRR29007558,SRX24534634,SRS21280317,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Hom 3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Hom3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Hom 3,Arfgef1 Hom 3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Hom_3_1.fq.gz Arfgef1_Hom_3_2.fq.gz,fastq fastq,7294731000.0,24315770.0,Arfgef1 Hom 3 1.fq.gz,0:150 1:150,A:1847018467;C:1809604703;G:1818278888;T:1819707786;N:121156,150,150,,,1847018467,1809604703,1818278888,1819707786,121156,SRX24534634,SRS21280317,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32070,SRR29007559,SRX24534633,SRS21280316,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Hom 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Hom2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Hom 2,Arfgef1 Hom 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Hom_2_1.fq.gz Arfgef1_Hom_2_2.fq.gz,fastq fastq,6607825200.0,22026084.0,Arfgef1 Hom 2 1.fq.gz,0:150 1:150,A:1694417387;C:1616938849;G:1625276704;T:1671046414;N:145846,150,150,,,1694417387,1616938849,1625276704,1671046414,145846,SRX24534633,SRS21280316,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32071,SRR29007560,SRX24534632,SRS21280315,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Hom 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Hom1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Hom 1,Arfgef1 Hom 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Hom_1_1.fq.gz Arfgef1_Hom_1_2.fq.gz,fastq fastq,6777738600.0,22592462.0,Arfgef1 Hom 1 1.fq.gz,0:150 1:150,A:1739306802;C:1658195023;G:1665806667;T:1714318423;N:111685,150,150,,,1739306802,1658195023,1665806667,1714318423,111685,SRX24534632,SRS21280315,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32072,SRR29007561,SRX24534631,SRS21280314,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Het 3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Het3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Het 3,Arfgef1 Het 3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Het_3_1.fq.gz Arfgef1_Het_3_2.fq.gz,fastq fastq,6739993500.0,22466645.0,Arfgef1 Het 3 1.fq.gz,0:150 1:150,A:1725253563;C:1652471358;G:1662793828;T:1699392429;N:82322,150,150,,,1725253563,1652471358,1662793828,1699392429,82322,SRX24534631,SRS21280314,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32073,SRR29007562,SRX24534630,SRS21280313,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Het 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Het2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Het 2,Arfgef1 Het 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Het_2_1.fq.gz Arfgef1_Het_2_2.fq.gz,fastq fastq,9510813000.0,31702710.0,Arfgef1 Het 2 1.fq.gz,0:150 1:150,A:2509621883;C:2259671963;G:2271899998;T:2469380560;N:238596,150,150,,,2509621883,2259671963,2271899998,2469380560,238596,SRX24534630,SRS21280313,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32074,SRR29007563,SRX24534629,SRS21280312,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Het 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Het1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Het 1,Arfgef1 Het 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Het_1_1.fq.gz Arfgef1_Het_1_2.fq.gz,fastq fastq,6887369100.0,22957897.0,Arfgef1 Het 1 1.fq.gz,0:150 1:150,A:1766549896;C:1685533018;G:1694949682;T:1740214059;N:122445,150,150,,,1766549896,1685533018,1694949682,1740214059,122445,SRX24534629,SRS21280312,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32075,SRR29007564,SRX24534628,SRS21280311,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Hom 3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Hom3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Hom 3,Wnt8b Hom 3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Hom_3_1.fq.gz Wnt8b_Hom_3_2.fq.gz,fastq fastq,10567857900.0,35226193.0,Wnt8b Hom 3 1.fq.gz,0:150 1:150,A:2775044850;C:2525957688;G:2527072827;T:2739479844;N:302691,150,150,,,2775044850,2525957688,2527072827,2739479844,302691,SRX24534628,SRS21280311,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32076,SRR29007565,SRX24534627,SRS21280310,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Hom 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Hom2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Hom 2,Wnt8b Hom 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Hom_2_1.fq.gz Wnt8b_Hom_2_2.fq.gz,fastq fastq,7666806600.0,25556022.0,Wnt8b Hom 2 1.fq.gz,0:150 1:150,A:2029345938;C:1820579149;G:1819606043;T:1996786660;N:488810,150,150,,,2029345938,1820579149,1819606043,1996786660,488810,SRX24534627,SRS21280310,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32077,SRR29007566,SRX24534626,SRS21280309,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Hom 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Hom1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Hom 1,Wnt8b Hom 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Hom_1_1.fq.gz Wnt8b_Hom_1_2.fq.gz,fastq fastq,6514544400.0,21715148.0,Wnt8b Hom 1 1.fq.gz,0:150 1:150,A:1711943699;C:1556010812;G:1555687818;T:1690731439;N:170632,150,150,,,1711943699,1556010812,1555687818,1690731439,170632,SRX24534626,SRS21280309,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32078,SRR29007567,SRX24534625,SRS21280308,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Het 3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Het3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Het 3,Wnt8b Het 3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Het_3_1.fq.gz Wnt8b_Het_3_2.fq.gz,fastq fastq,8714661900.0,29048873.0,Wnt8b Het 3 1.fq.gz,0:150 1:150,A:2360994905;C:2008091028;G:2013456743;T:2332006781;N:112443,150,150,,,2360994905,2008091028,2013456743,2332006781,112443,SRX24534625,SRS21280308,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32079,SRR29007568,SRX24534624,SRS21280307,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Het 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Het2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Het 2,Wnt8b Het 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Het_2_1.fq.gz Wnt8b_Het_2_2.fq.gz,fastq fastq,8370112800.0,27900376.0,Wnt8b Het 2 1.fq.gz,0:150 1:150,A:2275496039;C:1920819728;G:1927597917;T:2246091711;N:107405,150,150,,,2275496039,1920819728,1927597917,2246091711,107405,SRX24534624,SRS21280307,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32080,SRR29007569,SRX24534623,SRS21280306,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Het 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Het1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Het 1,Wnt8b Het 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Het_1_1.fq.gz Wnt8b_Het_1_2.fq.gz,fastq fastq,7614189000.0,25380630.0,Wnt8b Het 1 1.fq.gz,0:150 1:150,A:2059784093;C:1755740426;G:1761242316;T:2037325656;N:96509,150,150,,,2059784093,1755740426,1761242316,2037325656,96509,SRX24534623,SRS21280306,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32081,SRR29007570,SRX24534622,SRS21280305,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Wt 3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Wt3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Wt 3,Wnt8b Wt 3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Wt_3_1.fq.gz Wnt8b_Wt_3_2.fq.gz,fastq fastq,6809737500.0,22699125.0,Wnt8b Wt 3 1.fq.gz,0:150 1:150,A:1869159615;C:1548130956;G:1547169482;T:1845192460;N:84987,150,150,,,1869159615,1548130956,1547169482,1845192460,84987,SRX24534622,SRS21280305,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32082,SRR29007571,SRX24534621,SRS21280304,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Wt 3,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Wt3|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Wt 3,Arfgef1 Wt 3,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Wt_3_1.fq.gz Arfgef1_Wt_3_2.fq.gz,fastq fastq,6162364200.0,20541214.0,Arfgef1 Wt 3 1.fq.gz,0:150 1:150,A:1606427072;C:1484826935;G:1488745137;T:1582299135;N:65921,150,150,,,1606427072,1484826935,1488745137,1582299135,65921,SRX24534621,SRS21280304,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32083,SRR29007572,SRX24534620,SRS21280303,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Wt 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Wt2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Wt 2,Wnt8b Wt 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Wt_2_1.fq.gz Wnt8b_Wt_2_2.fq.gz,fastq fastq,6743670600.0,22478902.0,Wnt8b Wt 2 1.fq.gz,0:150 1:150,A:1852520280;C:1531023930;G:1536795067;T:1823243896;N:87427,150,150,,,1852520280,1531023930,1536795067,1823243896,87427,SRX24534620,SRS21280303,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32084,SRR29007573,SRX24534619,SRS21280302,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Wnt8b Wt 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Wnt8b Wt1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Wnt8b Wt 1,Wnt8b Wt 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Wnt8b_Wt_1_1.fq.gz Wnt8b_Wt_1_2.fq.gz,fastq fastq,6534620400.0,21782068.0,Wnt8b Wt 1 1.fq.gz,0:150 1:150,A:1783250074;C:1493088330;G:1497228073;T:1760957638;N:96285,150,150,,,1783250074,1493088330,1497228073,1760957638,96285,SRX24534619,SRS21280302,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32085,SRR29007574,SRX24534618,SRS21280301,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Hom 4,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Hom4|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Hom 4,Kcnd2 Hom 4,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Hom_4_1.fq.gz Kcnd2_Hom_4_2.fq.gz,fastq fastq,7596974100.0,25323247.0,Kcnd2 Hom 4 1.fq.gz,0:150 1:150,A:2007694949;C:1807188755;G:1800403701;T:1981369650;N:317045,150,150,,,2007694949,1807188755,1800403701,1981369650,317045,SRX24534618,SRS21280301,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32086,SRR29007575,SRX24534617,SRS21280300,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Hom 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Hom2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Hom 2,Kcnd2 Hom 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Hom_2_1.fq.gz Kcnd2_Hom_2_2.fq.gz,fastq fastq,7289261100.0,24297537.0,Kcnd2 Hom 2 1.fq.gz,0:150 1:150,A:2078143741;C:1581832453;G:1587225393;T:2041970189;N:89324,150,150,,,2078143741,1581832453,1587225393,2041970189,89324,SRX24534617,SRS21280300,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32087,SRR29007576,SRX24534616,SRS21280299,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Hom 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Hom1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Hom 1,Kcnd2 Hom 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Hom_1_1.fq.gz Kcnd2_Hom_1_2.fq.gz,fastq fastq,8331212400.0,27770708.0,Kcnd2 Hom 1 1.fq.gz,0:150 1:150,A:2185320924;C:1987553985;G:1999101969;T:2159195984;N:39538,150,150,,,2185320924,1987553985,1999101969,2159195984,39538,SRX24534616,SRS21280299,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32088,SRR29007577,SRX24534615,SRS21280298,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Het 4,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Het4|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Het 4,Kcnd2 Het 4,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Het_4_1.fq.gz Kcnd2_Het_4_2.fq.gz,fastq fastq,10195958700.0,33986529.0,Kcnd2 Het 4 1.fq.gz,0:150 1:150,A:2675050868;C:2442920285;G:2439165482;T:2638402351;N:419714,150,150,,,2675050868,2442920285,2439165482,2638402351,419714,SRX24534615,SRS21280298,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32089,SRR29007578,SRX24534614,SRS21280297,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Het 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Het2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Het 2,Kcnd2 Het 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Het_2_1.fq.gz Kcnd2_Het_2_2.fq.gz,fastq fastq,7549108800.0,25163696.0,Kcnd2 Het 2 1.fq.gz,0:150 1:150,A:1994641167;C:1795831385;G:1796069017;T:1962477823;N:89408,150,150,,,1994641167,1795831385,1796069017,1962477823,89408,SRX24534614,SRS21280297,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32090,SRR29007579,SRX24534613,SRS21280296,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Het 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Het1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Het 1,Kcnd2 Het 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Het_1_1.fq.gz Kcnd2_Het_1_2.fq.gz,fastq fastq,7081857600.0,23606192.0,Kcnd2 Het 1 1.fq.gz,0:150 1:150,A:1860484446;C:1694088253;G:1695161253;T:1832038793;N:84855,150,150,,,1860484446,1694088253,1695161253,1832038793,84855,SRX24534613,SRS21280296,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32091,SRR29007580,SRX24534612,SRS21280295,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Wt 4,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Wt4|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Wt 4,Kcnd2 Wt 4,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Wt_4_1.fq.gz Kcnd2_Wt_4_2.fq.gz,fastq fastq,8142446700.0,27141489.0,Kcnd2 Wt 4 1.fq.gz,0:150 1:150,A:2136890254;C:1951822302;G:1947544318;T:2105854363;N:335463,150,150,,,2136890254,1951822302,1947544318,2105854363,335463,SRX24534612,SRS21280295,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32092,SRR29007581,SRX24534611,SRS21280294,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Kcnd2 Wt 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Kcnd2 Wt2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Kcnd2 Wt 2,Kcnd2 Wt 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Kcnd2_Wt_2_1.fq.gz Kcnd2_Wt_2_2.fq.gz,fastq fastq,6688680600.0,22295602.0,Kcnd2 Wt 2 1.fq.gz,0:150 1:150,A:1902466623;C:1451301657;G:1460696794;T:1874184765;N:30761,150,150,,,1902466623,1451301657,1460696794,1874184765,30761,SRX24534611,SRS21280294,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32093,SRR29007582,SRX24534610,SRS21280293,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Wt 2,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Wt2|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Wt 2,Arfgef1 Wt 2,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Wt_2_1.fq.gz Arfgef1_Wt_2_2.fq.gz,fastq fastq,7399981500.0,24666605.0,Arfgef1 Wt 2 1.fq.gz,0:150 1:150,A:1904125951;C:1807905407;G:1812898141;T:1874904149;N:147852,150,150,,,1904125951,1807905407,1812898141,1874904149,147852,SRX24534610,SRS21280293,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32094,SRR29007583,SRX24534609,SRS21280292,SRP507312,PRJNA1111077,Zebrafish models of candidate human epilepsy associated genes provide evidence of hyperexcitability,PRJNA1111077,Other,Hundreds of novel candidate human epilepsy associated genes have been identified thanks to advancements in next generation sequencing and large genome wide association studies  but establishing genetic etiology requires functional validation. We generated a list of >2200 candidate epilepsy associated genes  of which 48 were developed into stable loss of function zebrafish models. Of those 48  evidence of seizure like behavior was present in 5 arfgef1  kcnd2  kcnv1  ubr5  wnt8b. Further characterization provided evidence for epileptiform activity via electrophysiology in kcnd2 and wnt8b mutants. Additionally  arfgef1 and wnt8b mutants showed a decrease in the number of inhibitory interneurons in the optic tectum of larval animals. Further  RNA Seq revealed convergent transcriptional abnormalities between mutant lines  consistent with their developmental defects and hyperexcitable phenotypes. These zebrafish models provide strongest experimental evidence supporting the role of ARFGEF1  KCND2  and WNT8B in human epilepsy and further demonstrate the utility of this model system for evaluating candidate human epilepsy genes.,,,,,Arfgef1 Wt 1,,strain:Casper|age:5dpf|collection date:2022 12 09|geo loc name:USA: Boston  MA|sex:not applicable|tissue:Head|genotype:Arfgef1 Wt1|BioSampleModel:Model organism or animal,,,,,,,,,RNA Seq of Danio Rerio: pools of isolated larval head,Arfgef1 Wt 1,Arfgef1 Wt 1,Three replicate larvae from Het in crosses  aged 5 dpf  were sacrificed on ice and stored in RNAlater Stabilization Solution according to product specifications. Larval heads were isolated from bodies  which were used for Sanger sequencing for genotyping. Heads were pooled in groups of 20 25 according to genotype and RNA was isolated using a Qiagen RNeasy plus kit according to specifications. QC was performed via Agilent 2100 bioanalyzer  and only samples with an RNA integrity number value of >5.8 were used for library preparation.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507312,,,Arfgef1_Wt_1_1.fq.gz Arfgef1_Wt_1_2.fq.gz,fastq fastq,7542057300.0,25140191.0,Arfgef1 Wt 1 1.fq.gz,0:150 1:150,A:1927852618;C:1855757148;G:1860100302;T:1898222485;N:124747,150,150,,,1927852618,1855757148,1860100302,1898222485,124747,SRX24534609,SRS21280292,SRA1864976,Boston Childrens Hospital|Neurobiology,Boston Childrens Hospital,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,United States,2024-05-13,Larval,Larval,Head,Nervous System
32098,SRR29008446,SRX24535482,SRS21281082,SRP507332,PRJNA1111082,Integration of ATAC and RNA Sequencing identifies chromatin and transcriptomic signatures in classical and non classical zebrafish osteoblasts and indicates mechanisms of entpd5a regulation [RNA],GSE267333,Transcriptome Analysis,Two types of osteoblasts are required to assemble the zebrafish embryonic skeleton: classical osteoblasts homologous to the mammalian situation  and notochord sheath cells  which serve as non classical osteoblasts. The gene entpd5a is critically required for ossification via both types of osteoblasts. Despite the usefulness of zebrafish models in vertebrate research  the genetic regulation of bone formation  as well as mechanisms of transcriptional control of entpd5a  remain largely unknown. Here  using a newly generated transgenic line  we isolate classical and non classical osteoblasts from zebrafish embryos and performed both ATAC Seq and RNA Seq. We analysed results independently and integratively to understand those chromatin dynamics and accompanying transcriptomic changes that occur in different skeletal cells. We show that although Dlx family factors are playing important roles in classical osteoblast regulation  Hox family factors are involved in governing spinal ossification via non classical osteoblasts. We further present a resource driven analysis of the entpd5a promoter  experimentally validating the ATAC Seq dataset and proposing mechanisms of regulating the complex entpd5a expression pattern during zebrafish osteogenesis. Our results thus provide a necessary comprehensive resource for the field of bone development and indicate spatio temporally regulated promoter/enhancer interactions taking place in the entpd5a locus. Overall design: We used the newly generated entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry transgenic line to isolate via FACS head classical and trunk non classical osteoblasts from zebrafish embryos at 15dpf. We also extracted adjacent head cartilage and intersegmental spinal chondrocytes as controls. With these four isolated cell populations we performed both ATAC Seq and RNA Seq and analysed data at first individually  to establish open chromatin regions and gene expression profiles  respectively. We then integrated the data to enable us to produce a list of candidate transcription factors likely to function in vivo in each of the cell types during zebrafish skeletogenesis.,,,,Chondrocyte head biolRep3,GSM8264152,,source name:head|tissue:head|cell type:head chondrocyte|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf loc name:missing|collection date:missing,Chondrocyte head biolRep3,QC of sequences  adapter trimming and duplicate removal using fastp package with   dedup option Sequence alignment to genome using the STAR aligner samtools to sort and index aligned reads reads counted using the featureCounts command from the Subread package Assembly: danRer11 Supplementary files format and content: tab deliminated text files including raw count for each sample 7th column,head,,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,tissue:head|cell type:head chondrocyte|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf,GSM8264152,GSM8264152: Chondrocyte head biolRep3; Danio rerio; RNA Seq,GSM8264152 r1,GSM8264152,1,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507332,,loader:fastq load.py,cartilRep3_R1.fastq.gz cartilRep3_R2.fastq.gz,fastq fastq,6819648393.0,25781563.0,GSM8264152 r1,0:132.28 1:132.24,A:1843991471;C:1548648708;G:1568393744;T:1858508350;N:106120,132,132,,,1843991471,1548648708,1568393744,1858508350,106120,SRX24535482,SRS21281082,SRA1865629,Institute for Cardiovascular Organogenesis and Regeneration,Institute for Cardiovascular Organogenesis and Regeneration,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Germany,2024-05-13,Larval,Larval,Head,Nervous System
32099,SRR29008447,SRX24535481,SRS21281081,SRP507332,PRJNA1111082,Integration of ATAC and RNA Sequencing identifies chromatin and transcriptomic signatures in classical and non classical zebrafish osteoblasts and indicates mechanisms of entpd5a regulation [RNA],GSE267333,Transcriptome Analysis,Two types of osteoblasts are required to assemble the zebrafish embryonic skeleton: classical osteoblasts homologous to the mammalian situation  and notochord sheath cells  which serve as non classical osteoblasts. The gene entpd5a is critically required for ossification via both types of osteoblasts. Despite the usefulness of zebrafish models in vertebrate research  the genetic regulation of bone formation  as well as mechanisms of transcriptional control of entpd5a  remain largely unknown. Here  using a newly generated transgenic line  we isolate classical and non classical osteoblasts from zebrafish embryos and performed both ATAC Seq and RNA Seq. We analysed results independently and integratively to understand those chromatin dynamics and accompanying transcriptomic changes that occur in different skeletal cells. We show that although Dlx family factors are playing important roles in classical osteoblast regulation  Hox family factors are involved in governing spinal ossification via non classical osteoblasts. We further present a resource driven analysis of the entpd5a promoter  experimentally validating the ATAC Seq dataset and proposing mechanisms of regulating the complex entpd5a expression pattern during zebrafish osteogenesis. Our results thus provide a necessary comprehensive resource for the field of bone development and indicate spatio temporally regulated promoter/enhancer interactions taking place in the entpd5a locus. Overall design: We used the newly generated entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry transgenic line to isolate via FACS head classical and trunk non classical osteoblasts from zebrafish embryos at 15dpf. We also extracted adjacent head cartilage and intersegmental spinal chondrocytes as controls. With these four isolated cell populations we performed both ATAC Seq and RNA Seq and analysed data at first individually  to establish open chromatin regions and gene expression profiles  respectively. We then integrated the data to enable us to produce a list of candidate transcription factors likely to function in vivo in each of the cell types during zebrafish skeletogenesis.,,,,Chondrocyte head biolRep2,GSM8264151,,source name:head|tissue:head|cell type:head chondrocyte|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf loc name:missing|collection date:missing,Chondrocyte head biolRep2,QC of sequences  adapter trimming and duplicate removal using fastp package with   dedup option Sequence alignment to genome using the STAR aligner samtools to sort and index aligned reads reads counted using the featureCounts command from the Subread package Assembly: danRer11 Supplementary files format and content: tab deliminated text files including raw count for each sample 7th column,head,,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,tissue:head|cell type:head chondrocyte|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf,GSM8264151,GSM8264151: Chondrocyte head biolRep2; Danio rerio; RNA Seq,GSM8264151 r1,GSM8264151,1,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507332,,loader:fastq load.py,cartilRep2_R1.fastq.gz cartilRep2_R2.fastq.gz,fastq fastq,6328377834.0,23616303.0,GSM8264151 r1,0:134.02 1:133.95,A:1697207927;C:1464700434;G:1476121489;T:1690068467;N:279517,134,133,,,1697207927,1464700434,1476121489,1690068467,279517,SRX24535481,SRS21281081,SRA1865629,Institute for Cardiovascular Organogenesis and Regeneration,Institute for Cardiovascular Organogenesis and Regeneration,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Germany,2024-05-13,Larval,Larval,Head,Nervous System
32100,SRR29008448,SRX24535480,SRS21281080,SRP507332,PRJNA1111082,Integration of ATAC and RNA Sequencing identifies chromatin and transcriptomic signatures in classical and non classical zebrafish osteoblasts and indicates mechanisms of entpd5a regulation [RNA],GSE267333,Transcriptome Analysis,Two types of osteoblasts are required to assemble the zebrafish embryonic skeleton: classical osteoblasts homologous to the mammalian situation  and notochord sheath cells  which serve as non classical osteoblasts. The gene entpd5a is critically required for ossification via both types of osteoblasts. Despite the usefulness of zebrafish models in vertebrate research  the genetic regulation of bone formation  as well as mechanisms of transcriptional control of entpd5a  remain largely unknown. Here  using a newly generated transgenic line  we isolate classical and non classical osteoblasts from zebrafish embryos and performed both ATAC Seq and RNA Seq. We analysed results independently and integratively to understand those chromatin dynamics and accompanying transcriptomic changes that occur in different skeletal cells. We show that although Dlx family factors are playing important roles in classical osteoblast regulation  Hox family factors are involved in governing spinal ossification via non classical osteoblasts. We further present a resource driven analysis of the entpd5a promoter  experimentally validating the ATAC Seq dataset and proposing mechanisms of regulating the complex entpd5a expression pattern during zebrafish osteogenesis. Our results thus provide a necessary comprehensive resource for the field of bone development and indicate spatio temporally regulated promoter/enhancer interactions taking place in the entpd5a locus. Overall design: We used the newly generated entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry transgenic line to isolate via FACS head classical and trunk non classical osteoblasts from zebrafish embryos at 15dpf. We also extracted adjacent head cartilage and intersegmental spinal chondrocytes as controls. With these four isolated cell populations we performed both ATAC Seq and RNA Seq and analysed data at first individually  to establish open chromatin regions and gene expression profiles  respectively. We then integrated the data to enable us to produce a list of candidate transcription factors likely to function in vivo in each of the cell types during zebrafish skeletogenesis.,,,,Chondrocyte head biolRep1,GSM8264150,,source name:head|tissue:head|cell type:head chondrocyte|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf loc name:missing|collection date:missing,Chondrocyte head biolRep1,QC of sequences  adapter trimming and duplicate removal using fastp package with   dedup option Sequence alignment to genome using the STAR aligner samtools to sort and index aligned reads reads counted using the featureCounts command from the Subread package Assembly: danRer11 Supplementary files format and content: tab deliminated text files including raw count for each sample 7th column,head,,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,tissue:head|cell type:head chondrocyte|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf,GSM8264150,GSM8264150: Chondrocyte head biolRep1; Danio rerio; RNA Seq,GSM8264150 r1,GSM8264150,1,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507332,,loader:fastq load.py,cartilRep1_R1.fastq.gz cartilRep1_R2.fastq.gz,fastq fastq,3594349367.0,13391209.0,GSM8264150 r1,0:134.24 1:134.17,A:956150712;C:837180050;G:846748291;T:954113728;N:156586,134,134,,,956150712,837180050,846748291,954113728,156586,SRX24535480,SRS21281080,SRA1865629,Institute for Cardiovascular Organogenesis and Regeneration,Institute for Cardiovascular Organogenesis and Regeneration,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Germany,2024-05-13,Larval,Larval,Head,Nervous System
32104,SRR29008452,SRX24535476,SRS21281076,SRP507332,PRJNA1111082,Integration of ATAC and RNA Sequencing identifies chromatin and transcriptomic signatures in classical and non classical zebrafish osteoblasts and indicates mechanisms of entpd5a regulation [RNA],GSE267333,Transcriptome Analysis,Two types of osteoblasts are required to assemble the zebrafish embryonic skeleton: classical osteoblasts homologous to the mammalian situation  and notochord sheath cells  which serve as non classical osteoblasts. The gene entpd5a is critically required for ossification via both types of osteoblasts. Despite the usefulness of zebrafish models in vertebrate research  the genetic regulation of bone formation  as well as mechanisms of transcriptional control of entpd5a  remain largely unknown. Here  using a newly generated transgenic line  we isolate classical and non classical osteoblasts from zebrafish embryos and performed both ATAC Seq and RNA Seq. We analysed results independently and integratively to understand those chromatin dynamics and accompanying transcriptomic changes that occur in different skeletal cells. We show that although Dlx family factors are playing important roles in classical osteoblast regulation  Hox family factors are involved in governing spinal ossification via non classical osteoblasts. We further present a resource driven analysis of the entpd5a promoter  experimentally validating the ATAC Seq dataset and proposing mechanisms of regulating the complex entpd5a expression pattern during zebrafish osteogenesis. Our results thus provide a necessary comprehensive resource for the field of bone development and indicate spatio temporally regulated promoter/enhancer interactions taking place in the entpd5a locus. Overall design: We used the newly generated entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry transgenic line to isolate via FACS head classical and trunk non classical osteoblasts from zebrafish embryos at 15dpf. We also extracted adjacent head cartilage and intersegmental spinal chondrocytes as controls. With these four isolated cell populations we performed both ATAC Seq and RNA Seq and analysed data at first individually  to establish open chromatin regions and gene expression profiles  respectively. We then integrated the data to enable us to produce a list of candidate transcription factors likely to function in vivo in each of the cell types during zebrafish skeletogenesis.,,,,Osteoblast head biolRep3,GSM8264146,,source name:head|tissue:head|cell type:osteoblast classical|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf loc name:missing|collection date:missing,Osteoblast head biolRep3,QC of sequences  adapter trimming and duplicate removal using fastp package with   dedup option Sequence alignment to genome using the STAR aligner samtools to sort and index aligned reads reads counted using the featureCounts command from the Subread package Assembly: danRer11 Supplementary files format and content: tab deliminated text files including raw count for each sample 7th column,head,,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,tissue:head|cell type:osteoblast classical|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf,GSM8264146,GSM8264146: Osteoblast head biolRep3; Danio rerio; RNA Seq,GSM8264146 r1,GSM8264146,1,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507332,,loader:fastq load.py,osteobRep3_R1.fastq.gz osteobRep3_R2.fastq.gz,fastq fastq,4016101824.0,15220140.0,GSM8264146 r1,0:131.95 1:131.92,A:1091466642;C:915105554;G:923772050;T:1085593417;N:164161,131,131,,,1091466642,915105554,923772050,1085593417,164161,SRX24535476,SRS21281076,SRA1865629,Institute for Cardiovascular Organogenesis and Regeneration,Institute for Cardiovascular Organogenesis and Regeneration,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Germany,2024-05-13,Larval,Larval,Head,Nervous System
32105,SRR29008453,SRX24535475,SRS21281075,SRP507332,PRJNA1111082,Integration of ATAC and RNA Sequencing identifies chromatin and transcriptomic signatures in classical and non classical zebrafish osteoblasts and indicates mechanisms of entpd5a regulation [RNA],GSE267333,Transcriptome Analysis,Two types of osteoblasts are required to assemble the zebrafish embryonic skeleton: classical osteoblasts homologous to the mammalian situation  and notochord sheath cells  which serve as non classical osteoblasts. The gene entpd5a is critically required for ossification via both types of osteoblasts. Despite the usefulness of zebrafish models in vertebrate research  the genetic regulation of bone formation  as well as mechanisms of transcriptional control of entpd5a  remain largely unknown. Here  using a newly generated transgenic line  we isolate classical and non classical osteoblasts from zebrafish embryos and performed both ATAC Seq and RNA Seq. We analysed results independently and integratively to understand those chromatin dynamics and accompanying transcriptomic changes that occur in different skeletal cells. We show that although Dlx family factors are playing important roles in classical osteoblast regulation  Hox family factors are involved in governing spinal ossification via non classical osteoblasts. We further present a resource driven analysis of the entpd5a promoter  experimentally validating the ATAC Seq dataset and proposing mechanisms of regulating the complex entpd5a expression pattern during zebrafish osteogenesis. Our results thus provide a necessary comprehensive resource for the field of bone development and indicate spatio temporally regulated promoter/enhancer interactions taking place in the entpd5a locus. Overall design: We used the newly generated entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry transgenic line to isolate via FACS head classical and trunk non classical osteoblasts from zebrafish embryos at 15dpf. We also extracted adjacent head cartilage and intersegmental spinal chondrocytes as controls. With these four isolated cell populations we performed both ATAC Seq and RNA Seq and analysed data at first individually  to establish open chromatin regions and gene expression profiles  respectively. We then integrated the data to enable us to produce a list of candidate transcription factors likely to function in vivo in each of the cell types during zebrafish skeletogenesis.,,,,Osteoblast head biolRep2,GSM8264145,,source name:head|tissue:head|cell type:osteoblast classical|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf loc name:missing|collection date:missing,Osteoblast head biolRep2,QC of sequences  adapter trimming and duplicate removal using fastp package with   dedup option Sequence alignment to genome using the STAR aligner samtools to sort and index aligned reads reads counted using the featureCounts command from the Subread package Assembly: danRer11 Supplementary files format and content: tab deliminated text files including raw count for each sample 7th column,head,,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,tissue:head|cell type:osteoblast classical|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf,GSM8264145,GSM8264145: Osteoblast head biolRep2; Danio rerio; RNA Seq,GSM8264145 r1,GSM8264145,1,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507332,,loader:fastq load.py,osteobRep2_R1.fastq.gz osteobRep2_R2.fastq.gz,fastq fastq,3692172504.0,14317610.0,GSM8264145 r1,0:128.95 1:128.93,A:1007186967;C:837532125;G:846083342;T:1001209204;N:160866,128,128,,,1007186967,837532125,846083342,1001209204,160866,SRX24535475,SRS21281075,SRA1865629,Institute for Cardiovascular Organogenesis and Regeneration,Institute for Cardiovascular Organogenesis and Regeneration,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Germany,2024-05-13,Larval,Larval,Head,Nervous System
32106,SRR29008454,SRX24535474,SRS21281074,SRP507332,PRJNA1111082,Integration of ATAC and RNA Sequencing identifies chromatin and transcriptomic signatures in classical and non classical zebrafish osteoblasts and indicates mechanisms of entpd5a regulation [RNA],GSE267333,Transcriptome Analysis,Two types of osteoblasts are required to assemble the zebrafish embryonic skeleton: classical osteoblasts homologous to the mammalian situation  and notochord sheath cells  which serve as non classical osteoblasts. The gene entpd5a is critically required for ossification via both types of osteoblasts. Despite the usefulness of zebrafish models in vertebrate research  the genetic regulation of bone formation  as well as mechanisms of transcriptional control of entpd5a  remain largely unknown. Here  using a newly generated transgenic line  we isolate classical and non classical osteoblasts from zebrafish embryos and performed both ATAC Seq and RNA Seq. We analysed results independently and integratively to understand those chromatin dynamics and accompanying transcriptomic changes that occur in different skeletal cells. We show that although Dlx family factors are playing important roles in classical osteoblast regulation  Hox family factors are involved in governing spinal ossification via non classical osteoblasts. We further present a resource driven analysis of the entpd5a promoter  experimentally validating the ATAC Seq dataset and proposing mechanisms of regulating the complex entpd5a expression pattern during zebrafish osteogenesis. Our results thus provide a necessary comprehensive resource for the field of bone development and indicate spatio temporally regulated promoter/enhancer interactions taking place in the entpd5a locus. Overall design: We used the newly generated entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry transgenic line to isolate via FACS head classical and trunk non classical osteoblasts from zebrafish embryos at 15dpf. We also extracted adjacent head cartilage and intersegmental spinal chondrocytes as controls. With these four isolated cell populations we performed both ATAC Seq and RNA Seq and analysed data at first individually  to establish open chromatin regions and gene expression profiles  respectively. We then integrated the data to enable us to produce a list of candidate transcription factors likely to function in vivo in each of the cell types during zebrafish skeletogenesis.,,,,Osteoblast head biolRep1,GSM8264144,,source name:head|tissue:head|cell type:osteoblast classical|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf loc name:missing|collection date:missing,Osteoblast head biolRep1,QC of sequences  adapter trimming and duplicate removal using fastp package with   dedup option Sequence alignment to genome using the STAR aligner samtools to sort and index aligned reads reads counted using the featureCounts command from the Subread package Assembly: danRer11 Supplementary files format and content: tab deliminated text files including raw count for each sample 7th column,head,,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,tissue:head|cell type:osteoblast classical|genotype:WT; entpd5a:Gal4FF;UAS:GFP;R2col2a1a:mCherry|Stage:15 dpf,GSM8264144,GSM8264144: Osteoblast head biolRep1; Danio rerio; RNA Seq,GSM8264144 r1,GSM8264144,1,RNA was isolated using the RNeasy Plus Micro Kit QIAGEN  74034. Samples were sent to Eurofins Genomics for library preparation and paired end sequencing with the INVIEW Transcriptome Ultra Low service 2x 150. Per sample  15M reads were sequenced.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina NovaSeq 6000,,SRP507332,,loader:fastq load.py,osteobRep1_R1.fastq.gz osteobRep1_R2.fastq.gz,fastq fastq,8569394356.0,28375478.0,GSM8264144 r1,0:151 1:151,A:2308551585;C:1841082082;G:2161425693;T:2253505108;N:4829888,151,151,,,2308551585,1841082082,2161425693,2253505108,4829888,SRX24535474,SRS21281074,SRA1865629,Institute for Cardiovascular Organogenesis and Regeneration,Institute for Cardiovascular Organogenesis and Regeneration,,,,,,,,,,,,B,B,biological fallback assumption,illumina,novaseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Germany,2024-05-13,Larval,Larval,Head,Nervous System
33619,SRR30310487,SRX25770932,SRS22407035,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,DM biol rep 3,GSM8473259,,source name:heads|tissue:heads|genotype:5a / ;5b / |treatment:untreated|geo loc name:missing|collection date:missing,DM biol rep 3,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5a / ;5b / |treatment:untreated,GSM8473259,GSM8473259: DM biol rep 3; Danio rerio; RNA Seq,GSM8473259 r1,GSM8473259,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47814-DM3_S6_R2_001.fastq.gz Li47814-DM3_S6_R1_001.fastq.gz,fastq fastq,4759652497.0,39356384.0,GSM8473259 r1,0:60.49 1:60.44,A:1221224093;C:1133209753;G:1144876807;T:1252303477;N:8038367,60,60,,,1221224093,1133209753,1144876807,1252303477,8038367,SRX25770932,SRS22407035,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94992,0.95405,0.07666,0.07486,0.64969,0.648,0.47911,0.48137,61,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33620,SRR30310488,SRX25770931,SRS22407034,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,DM biol rep 2,GSM8473258,,source name:heads|tissue:heads|genotype:5a / ;5b / |treatment:untreated|geo loc name:missing|collection date:missing,DM biol rep 2,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5a / ;5b / |treatment:untreated,GSM8473258,GSM8473258: DM biol rep 2; Danio rerio; RNA Seq,GSM8473258 r1,GSM8473258,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47813-DM2_S5_R2_001.fastq.gz Li47813-DM2_S5_R1_001.fastq.gz,fastq fastq,5030260806.0,41607672.0,GSM8473258 r1,0:60.47 1:60.43,A:1291665135;C:1198581962;G:1206075180;T:1323425262;N:10513267,60,60,,,1291665135,1198581962,1206075180,1323425262,10513267,SRX25770931,SRS22407034,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94958,0.95221,0.08402,0.0824,0.64628,0.64553,0.47628,0.47968,61,60,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33621,SRR30310489,SRX25770930,SRS22407033,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,DM biol rep 1,GSM8473257,,source name:heads|tissue:heads|genotype:5a / ;5b / |treatment:untreated|geo loc name:missing|collection date:missing,DM biol rep 1,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5a / ;5b / |treatment:untreated,GSM8473257,GSM8473257: DM biol rep 1; Danio rerio; RNA Seq,GSM8473257 r1,GSM8473257,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47812-DM1_S4_R2_001.fastq.gz Li47812-DM1_S4_R1_001.fastq.gz,fastq fastq,5442095245.0,45006091.0,GSM8473257 r1,0:60.48 1:60.44,A:1406768036;C:1288396960;G:1297715980;T:1439122995;N:10091274,60,60,,,1406768036,1288396960,1297715980,1439122995,10091274,SRX25770930,SRS22407033,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94722,0.95046,0.09788,0.09612,0.63984,0.6411,0.46913,0.4759,61,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33622,SRR30310490,SRX25770929,SRS22407032,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,5b biol rep 3,GSM8473256,,source name:heads|tissue:heads|genotype:5b / |treatment:untreated|geo loc name:missing|collection date:missing,5b biol rep 3,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5b / |treatment:untreated,GSM8473256,GSM8473256: 5b biol rep 3; Danio rerio; RNA Seq,GSM8473256 r1,GSM8473256,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47820-5b3_S12_R2_001.fastq.gz Li47820-5b3_S12_R1_001.fastq.gz,fastq fastq,5532330845.0,45739498.0,GSM8473256 r1,0:60.50 1:60.46,A:1435251569;C:1304605813;G:1312598084;T:1471267089;N:8608290,60,60,,,1435251569,1304605813,1312598084,1471267089,8608290,SRX25770929,SRS22407032,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94396,0.94717,0.11216,0.11051,0.64717,0.64768,0.47525,0.47841,60,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33623,SRR30310491,SRX25770928,SRS22407031,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,5b biol rep 2,GSM8473255,,source name:heads|tissue:heads|genotype:5b / |treatment:untreated|geo loc name:missing|collection date:missing,5b biol rep 2,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5b / |treatment:untreated,GSM8473255,GSM8473255: 5b biol rep 2; Danio rerio; RNA Seq,GSM8473255 r1,GSM8473255,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47819-5b2_S11_R2_001.fastq.gz Li47819-5b2_S11_R1_001.fastq.gz,fastq fastq,5530076725.0,45717614.0,GSM8473255 r1,0:60.50 1:60.46,A:1432780615;C:1306496067;G:1314858379;T:1467817877;N:8123787,60,60,,,1432780615,1306496067,1314858379,1467817877,8123787,SRX25770928,SRS22407031,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94205,0.94641,0.11508,0.11379,0.64788,0.64672,0.47602,0.47695,61,59,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33624,SRR30310492,SRX25770927,SRS22407030,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,5b biol rep 1,GSM8473254,,source name:heads|tissue:heads|genotype:5b / |treatment:untreated|geo loc name:missing|collection date:missing,5b biol rep 1,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5b / |treatment:untreated,GSM8473254,GSM8473254: 5b biol rep 1; Danio rerio; RNA Seq,GSM8473254 r1,GSM8473254,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47818-5b1_S10_R2_001.fastq.gz Li47818-5b1_S10_R1_001.fastq.gz,fastq fastq,4784996431.0,39556747.0,GSM8473254 r1,0:60.50 1:60.46,A:1241886071;C:1129207908;G:1136918789;T:1270031996;N:6951667,60,60,,,1241886071,1129207908,1136918789,1270031996,6951667,SRX25770927,SRS22407030,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94373,0.94771,0.11067,0.10905,0.64729,0.64583,0.47752,0.47625,59,60,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33625,SRR30310493,SRX25770926,SRS22407029,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,5a biol rep 3,GSM8473253,,source name:heads|tissue:heads|genotype:5a / |treatment:untreated|geo loc name:missing|collection date:missing,5a biol rep 3,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5a / |treatment:untreated,GSM8473253,GSM8473253: 5a biol rep 3; Danio rerio; RNA Seq,GSM8473253 r1,GSM8473253,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47817-5a3_S9_R2_001.fastq.gz Li47817-5a3_S9_R1_001.fastq.gz,fastq fastq,5455669007.0,45101219.0,GSM8473253 r1,0:60.51 1:60.46,A:1408981430;C:1292361893;G:1307301180;T:1439131814;N:7892690,60,60,,,1408981430,1292361893,1307301180,1439131814,7892690,SRX25770926,SRS22407029,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.95182,0.95421,0.081,0.07901,0.6524,0.65115,0.48336,0.48307,61,59,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33626,SRR30310494,SRX25770925,SRS22407028,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,5a biol rep 2,GSM8473252,,source name:heads|tissue:heads|genotype:5a / |treatment:untreated|geo loc name:missing|collection date:missing,5a biol rep 2,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5a / |treatment:untreated,GSM8473252,GSM8473252: 5a biol rep 2; Danio rerio; RNA Seq,GSM8473252 r1,GSM8473252,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47816-5a2_S8_R2_001.fastq.gz Li47816-5a2_S8_R1_001.fastq.gz,fastq fastq,5585703633.0,46182982.0,GSM8473252 r1,0:60.50 1:60.45,A:1439568272;C:1324867892;G:1340137608;T:1471972622;N:9157239,60,60,,,1439568272,1324867892,1340137608,1471972622,9157239,SRX25770925,SRS22407028,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.95103,0.95419,0.0813,0.07916,0.6565,0.65563,0.47441,0.47598,61,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33627,SRR30310495,SRX25770924,SRS22407027,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,5a biol rep 1,GSM8473251,,source name:heads|tissue:heads|genotype:5a /  |treatment:untreated|geo loc name:missing|collection date:missing,5a biol rep 1,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:5a /  |treatment:untreated,GSM8473251,GSM8473251: 5a biol rep 1; Danio rerio; RNA Seq,GSM8473251 r1,GSM8473251,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47815-5a1_S7_R2_001.fastq.gz Li47815-5a1_S7_R1_001.fastq.gz,fastq fastq,5421245773.0,44832660.0,GSM8473251 r1,0:60.48 1:60.44,A:1406624107;C:1276257498;G:1288190603;T:1440236606;N:9936959,60,60,,,1406624107,1276257498,1288190603,1440236606,9936959,SRX25770924,SRS22407027,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.9497,0.95318,0.08896,0.08766,0.64983,0.65009,0.46836,0.46856,60,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33628,SRR30310496,SRX25770923,SRS22407026,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,WT biol rep 3,GSM8473250,,source name:heads|tissue:heads|genotype:WT|treatment:untreated|geo loc name:missing|collection date:missing,WT biol rep 3,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:WT|treatment:untreated,GSM8473250,GSM8473250: WT biol rep 3; Danio rerio; RNA Seq,GSM8473250 r1,GSM8473250,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47811-WT3_S3_R2_001.fastq.gz Li47811-WT3_S3_R1_001.fastq.gz,fastq fastq,5445129556.0,45027951.0,GSM8473250 r1,0:60.48 1:60.45,A:1410861744;C:1282813821;G:1294884711;T:1446863056;N:9706224,60,60,,,1410861744,1282813821,1294884711,1446863056,9706224,SRX25770923,SRS22407026,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94943,0.95269,0.11544,0.11414,0.64644,0.64699,0.46439,0.47415,61,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33629,SRR30310497,SRX25770922,SRS22407025,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,WT biol rep 2,GSM8473249,,source name:heads|tissue:heads|genotype:WT|treatment:untreated|geo loc name:missing|collection date:missing,WT biol rep 2,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:WT|treatment:untreated,GSM8473249,GSM8473249: WT biol rep 2; Danio rerio; RNA Seq,GSM8473249 r1,GSM8473249,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47810-WT2_S2_R2_001.fastq.gz Li47810-WT2_S2_R1_001.fastq.gz,fastq fastq,4788359140.0,39599012.0,GSM8473249 r1,0:60.48 1:60.44,A:1237189996;C:1129331953;G:1143753687;T:1268980159;N:9103345,60,60,,,1237189996,1129331953,1143753687,1268980159,9103345,SRX25770922,SRS22407025,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94746,0.95043,0.1121,0.11092,0.64411,0.64342,0.46922,0.47301,59,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
33630,SRR30310498,SRX25770921,SRS22407024,SRP527479,PRJNA1150074,Epileptic phenotypes in slc13a5 loss of function zebrafish are rescued by blocking NMDA receptor signaling,GSE275235,Transcriptome Analysis,SLC13A5 encodes a citrate transporter highly expressed in the brain important for regulating intra  and extracellular citrate levels. Mutations in this gene cause a rare infantile epilepsy characterized by lifelong seizures  developmental delays  behavioral deficits  poor motor progression  and language impairments. SLC13A5 individuals respond poorly to treatment options; yet drug discovery programs are limited due to a paucity of animal models that phenocopy human symptoms. Here  we used CRISPR/Cas9 to create loss of function mutations in slc13a5a and slc13a5b  the zebrafish paralogs to human SLC13A5. slc13a5 mutant larvae showed cognitive dysfunction and sleep disturbances  consistent with SLC13A5 individuals. These mutants also exhibited fewer neurons and a concomitant increase in apoptosis across the optic tectum  a region important for sensory processing. slc13a5 mutants displayed hallmark features of epilepsy  including an imbalance in glutamatergic and GABAergic excitatory inhibitory gene expression  disrupted neurometabolism  and neuronal hyperexcitation as measured in vivo by extracellular field recordings and live calcium imaging. Mechanistically  we tested the involvement of NMDA signaling in slc13a5 mutant epilepsy like phenotypes. Slc13a5 protein co localizes with excitatory NMDA receptors in wild type zebrafish and blocking NMDA receptors in slc13a5 mutant larvae rescued bioenergetics  hyperexcitable calcium events  and behavioral defects. These data provide empirical evidence in support of the hypothesis that excess extracellular citrate over chelates the ions needed to regulate NMDA receptor function  leading to sustained channel opening and an exaggerated excitatory response that manifests as seizures. These data show the utility of slc13a5 mutant zebrafish for studying SLC13A5 epilepsy and open new avenues for drug discovery. Overall design: 5 dpf zebrafish heads were pooled to generate three biological replicates of each group. Four groups of samples were generated: WT controls  5a mutants  5b mutants and 5a/5b double mutants,,pubmed:40208862,,WT biol rep 1,GSM8473248,,source name:heads|tissue:heads|genotype:WT|treatment:untreated|geo loc name:missing|collection date:missing,WT biol rep 1,Fastq files were aligned using STAR and gene counts obtained from STAR were given as input to DESeq2 for differential gene analysis and obtained normalised counts. Genes with zero values in more than 4 samples were exlcuded from the analysis Assembly: GRCz11 Supplementary files format and content: tab delimited text file include raw counts for each sample Supplementary files format and content: tab delimited text file include log normalised counts for each sample,heads,untreated,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,Adult zebrafish TL and AB strains were maintained at 28°C in a 14 hour light/10 hour dark cycle under standard aquaculture conditions  and fertilized eggs were collected via natural spawning.,tissue:heads|genotype:WT|treatment:untreated,GSM8473248,GSM8473248: WT biol rep 1; Danio rerio; RNA Seq,GSM8473248 r1,GSM8473248,1,Trizol based RNA extraction and column purification purified RNA with RIN>7 were sent for sequencing NextSeq2000 P2 100 cycle,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,NextSeq 2000,,SRP527479,,,Li47809-WT1_S1_R2_001.fastq.gz Li47809-WT1_S1_R1_001.fastq.gz,fastq fastq,5047587318.0,41741097.0,GSM8473248 r1,0:60.48 1:60.44,A:1311031310;C:1185882586;G:1198272234;T:1343072853;N:9328335,60,60,,,1311031310,1185882586,1198272234,1343072853,9328335,SRX25770921,SRS22407024,SRA1951631,"Kurrasch Lab, Department of Medical Genetics, University of Calgary","Kurrasch Lab, Department of Medical Genetics, University of Calgary",2,0.94688,0.95005,0.12622,0.12476,0.6463,0.64528,0.47305,0.47428,61,61,B,B,biological fallback assumption,illumina,nextseq_v2,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Canada,2024-08-20,Adult,Adult,Head,Nervous System
36479,SRR527834,SRX171221,SRS352107,SRP014596,PRJNA171539,Transcriptomic analysis of zebrafish during development and homeostasis,GSE39703,Transcriptome Analysis,Sequencing libraries were generated from total RNA samples following the mRNAseq protocol for the generation of single end 16 hpf 36 hpf  5 day larvae  adult head and adult tail or paired end 24 hpf libraries Illumina. Single end reads of 36 nucleotides and paired end reads 2 x 76 nucleotides were obtained with a GAIIx Illumina. Gene expression at the different stages/tissu was assessed by cufflinks and HTseq. Overall design: RNAseq on 5 differents samples:  24hpf embryos  pool of 16 hour to 36 hour embryos  5 dpf larvea  adult head and adult tail,,pubmed:23684812,,head,GSM977959,,tissue:entire adult head|genotype:Wild type|strain:AB|Stage:adult head,head,Basecalls performed using CASAVA version 1.4 Reads aligned to zebrafish genome Zv9 Ensembl with Tophat v 1.4.1 and Bowtie v 0.12.7  options: butterfly search coverage search  microexon search  min anchor length 5   G GTF Determination of raw reads aligned to ZV9 with HTSeq v0.5.3p3 and gtf file ensembl zv9 release 60 Determination of RPKM/FPKM with cufflinks v 1.3.0 with the options  u  b  M rRNA/Mtgenes mask  G gtf Genome build: Zv9 v 60 Supplementary files format and content: *.count file are the output of Htseq reads quantification. *.fpkm files are the output of cufflinks quantification,entire adult head,,Extraction of total RNA with Trizol following manufacturer's instruction. Generation of mRNA libraries with Trueseq RNA kit following Illumina's instructions,,genotype:Wild type|strain:AB|Stage:adult head,GSM977959,GSM977959: head; Danio rerio; RNA Seq,GSM977959 1,GSM977959: head,1,,GEO Accession:GSM977959,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina Genome Analyzer IIx,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>36</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP014596,,,,,516054600.0,14334850.0,GSM977959 r1,0:36,A:144148482;C:115800670;G:121205261;T:134746787;N:153400,36,,,,144148482,115800670,121205261,134746787,153400,SRX171221,SRS352107,SRA056408,GEO,ITG,1,0.89668,,0.12577,,0.66803,,0.45871,,36,,B,,usable mapping rate,illumina,early_illumina,unknown,cdna_unspecified,trueseq,bulk,unknown,unknown,,Unknown,2012-07-27,Adult,Adult,Head,Nervous System
37210,SRR1028004,SRX376581,SRS501207,SRP032838,PRJNA227277,Danio rerio Transcriptome or Gene expression,PRJNA227277,Other,transcriptome analysis of zebrafish whole head.,,,wild type zebrafish sample 3,Wt 3,iiina,,label:3|age:6 days|tissue type:whole head,,,,,,,,,Transcriptome analysis of zebrafish's whole head.,ZF na   iiina,1,1,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2000,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>202</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC><READ_SPEC><READ_INDEX>1</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Reverse</READ_TYPE><BASE_COORD>102</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP032838,,,iiina_1.fastq.tar.gz iiina_2.fastq.tar.gz,fastq fastq,4316715356.0,21369878.0,iiina,0:101 1:101,A:1146719253;C:995646710;G:1009198100;T:1125396496;N:39754797,101,101,,,1146719253,995646710,1009198100,1125396496,39754797,SRX376581,SRS501207,SRA110728,BIU|Levanon,BIU,2,0.92916,0.92726,0.08723,0.0948,0.65514,0.68923,0.47003,0.47006,101,101,B,B,biological fallback assumption,illumina,hiseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Israel,2014-11-11,Larval,Larval,Head,Nervous System
37211,SRR1028003,SRX376580,SRS501206,SRP032838,PRJNA227277,Danio rerio Transcriptome or Gene expression,PRJNA227277,Other,transcriptome analysis of zebrafish whole head.,,,wild type zebrafish sample 2,Wt 2,iina,,label:2|age:6 days|tissue type:whole head,,,,,,,,,Transcriptome analysis of zebrafish's whole head.,ZF na   iina,1,1,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2000,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>202</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC><READ_SPEC><READ_INDEX>1</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Reverse</READ_TYPE><BASE_COORD>102</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP032838,,,iina_1.fastq.tar.gz iina_2.fastq.tar.gz,fastq fastq,4955839518.0,24533859.0,iina,0:101 1:101,A:1280850150;C:1179933762;G:1174869989;T:1275240888;N:44944729,101,101,,,1280850150,1179933762,1174869989,1275240888,44944729,SRX376580,SRS501206,SRA110728,BIU|Levanon,BIU,2,0.93499,0.9343,0.07143,0.07615,0.65427,0.67233,0.47221,0.47326,101,101,B,B,biological fallback assumption,illumina,hiseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Israel,2014-11-11,Larval,Larval,Head,Nervous System
37212,SRR1028002,SRX375515,SRS501219,SRP032838,PRJNA227277,Danio rerio Transcriptome or Gene expression,PRJNA227277,Other,transcriptome analysis of zebrafish whole head.,,,wild type zebrafish sample 1,Wt 1,ina,,label:1|age:6 days|tissue type:whole head,,,,,,,,,Transcriptome analysis of zebrafish's whole head.,ZF na   ina,1,1,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2000,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>202</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC><READ_SPEC><READ_INDEX>1</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Reverse</READ_TYPE><BASE_COORD>102</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP032838,,,ina_2.fastq.tar.gz ina_1.fastq.tar.gz,fastq fastq,5519994006.0,27326703.0,ina 1,0:101 1:101,A:1456361266;C:1288156090;G:1276246591;T:1448748282;N:50481777,101,101,,,1456361266,1288156090,1276246591,1448748282,50481777,SRX375515,SRS501219,SRA110728,BIU|Levanon,BIU,2,0.92874,0.9272,0.08523,0.09251,0.65445,0.67681,0.47526,0.47863,101,101,B,B,biological fallback assumption,illumina,hiseq_era,unknown,cdna_unspecified,unknown,bulk,unknown,unknown,,Israel,2014-11-11,Larval,Larval,Head,Nervous System
38299,SRR1648856,SRX757983,SRS743130,SRP049716,PRJNA266970,RNA sequencing of the developing zebrafish head,GSE63191,Transcriptome Analysis,We sequenced strand specific mRNA from the heads of 3 groups of wild type zebrafish Danio rerio 5 dpf Overall design: Examination of the relative expression of genes in the developing zebrafish brain,,pubmed:25561519,,Wildtype Replicate 3,GSM1543674,,source name:whole head|develolpmental stage:5 dpf embryo|tissue:whole head,Wildtype Replicate 3,Basecalls performed using CASAVA version 1.5 Alignment was performed with Gsnap v2012 07 20 using default parameters and the zv9 genome/transcriptome from Ensembl Accurate dose response was verified with custom analysis tools and the included ERCC RNA spike ins Aligned reads were quantified with Cufflinks v2.1.0 using default parameters and the zv9 transcriptome from Ensembl Genome build: zv9 Supplementary files format and content: Cufflinks v2.1.0 genes.fpkm tracking,whole head,,TRIzol Invitrogen extraction per manufactor's instructions Strand specific  polyA selected RNA Seq libraries were constructed using a custom dUTP method similar to the standard Illumina protocols  with the addition of 1ul of a 1:10 dilution of ERCC RNA spike ins prior to polyA selection.,Zebrafish embryos from natural matings were maintained at 28C in 6 or 10cm dishes. 5 dpf  the heads of 80 100 embryos per replicate were obtained for RNA extraction.,develolpmental stage:5 dpf embryo|tissue:whole head,GSM1543674,GSM1543674: Wildtype Replicate 3; Danio rerio; RNA Seq,GSM1543674,,1,TRIzol Invitrogen extraction per manufactor's instructions Strand specific  polyA selected RNA Seq libraries were constructed using a custom dUTP method similar to the standard Illumina protocols  with the addition of 1ul of a 1:10 dilution of ERCC RNA spike ins prior to polyA selection.,GEO Accession:GSM1543674,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2000,,SRP049716,,,uninjected_rep3_zebrafish_121230_AC1BMGACXX_Illumina8_1.fastq.gz uninjected_rep3_zebrafish_121230_AC1BMGACXX_Illumina8_2.fastq.gz,fastq fastq,7947025900.0,79470259.0,GSM1543674 r1,0:50 1:50,A:2171440033;C:1752204345;G:1782154451;T:2240911661;N:315410,50,50,,,2171440033,1752204345,1782154451,2240911661,315410,SRX757983,SRS743130,SRA200859,GEO,"Center for Human Genetic Research, Massachusetts General Hospital",2,0.92472,0.92889,0.15282,0.15037,0.72015,0.71969,0.47465,0.48174,50,50,B,B,biological fallback assumption,illumina,hiseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,United States,2014-11-12,Larval,Larval,Head,Nervous System
38300,SRR1648855,SRX757982,SRS743129,SRP049716,PRJNA266970,RNA sequencing of the developing zebrafish head,GSE63191,Transcriptome Analysis,We sequenced strand specific mRNA from the heads of 3 groups of wild type zebrafish Danio rerio 5 dpf Overall design: Examination of the relative expression of genes in the developing zebrafish brain,,pubmed:25561519,,Wildtype Replicate 2,GSM1543673,,source name:whole head|develolpmental stage:5 dpf embryo|tissue:whole head,Wildtype Replicate 2,Basecalls performed using CASAVA version 1.5 Alignment was performed with Gsnap v2012 07 20 using default parameters and the zv9 genome/transcriptome from Ensembl Accurate dose response was verified with custom analysis tools and the included ERCC RNA spike ins Aligned reads were quantified with Cufflinks v2.1.0 using default parameters and the zv9 transcriptome from Ensembl Genome build: zv9 Supplementary files format and content: Cufflinks v2.1.0 genes.fpkm tracking,whole head,,TRIzol Invitrogen extraction per manufactor's instructions Strand specific  polyA selected RNA Seq libraries were constructed using a custom dUTP method similar to the standard Illumina protocols  with the addition of 1ul of a 1:10 dilution of ERCC RNA spike ins prior to polyA selection.,Zebrafish embryos from natural matings were maintained at 28C in 6 or 10cm dishes. 5 dpf  the heads of 80 100 embryos per replicate were obtained for RNA extraction.,develolpmental stage:5 dpf embryo|tissue:whole head,GSM1543673,GSM1543673: Wildtype Replicate 2; Danio rerio; RNA Seq,GSM1543673,,1,TRIzol Invitrogen extraction per manufactor's instructions Strand specific  polyA selected RNA Seq libraries were constructed using a custom dUTP method similar to the standard Illumina protocols  with the addition of 1ul of a 1:10 dilution of ERCC RNA spike ins prior to polyA selection.,GEO Accession:GSM1543673,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2000,,SRP049716,,,uninjected_rep2_zebrafish_121230_AC1BMGACXX_Illumina5_2.fastq.gz uninjected_rep2_zebrafish_121230_AC1BMGACXX_Illumina5_1.fastq.gz,fastq fastq,7400831800.0,74008318.0,GSM1543673 r1,0:50 1:50,A:1997686488;C:1645601571;G:1723353684;T:2033898648;N:291409,50,50,,,1997686488,1645601571,1723353684,2033898648,291409,SRX757982,SRS743129,SRA200859,GEO,"Center for Human Genetic Research, Massachusetts General Hospital",2,0.90663,0.91107,0.33386,0.33587,0.7153,0.71553,0.48819,0.49079,50,50,B,B,biological fallback assumption,illumina,hiseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,United States,2014-11-12,Larval,Larval,Head,Nervous System
38301,SRR1648854,SRX757981,SRS743128,SRP049716,PRJNA266970,RNA sequencing of the developing zebrafish head,GSE63191,Transcriptome Analysis,We sequenced strand specific mRNA from the heads of 3 groups of wild type zebrafish Danio rerio 5 dpf Overall design: Examination of the relative expression of genes in the developing zebrafish brain,,pubmed:25561519,,Wildtype Replicate 1,GSM1543672,,source name:whole head|develolpmental stage:5 dpf embryo|tissue:whole head,Wildtype Replicate 1,Basecalls performed using CASAVA version 1.5 Alignment was performed with Gsnap v2012 07 20 using default parameters and the zv9 genome/transcriptome from Ensembl Accurate dose response was verified with custom analysis tools and the included ERCC RNA spike ins Aligned reads were quantified with Cufflinks v2.1.0 using default parameters and the zv9 transcriptome from Ensembl Genome build: zv9 Supplementary files format and content: Cufflinks v2.1.0 genes.fpkm tracking,whole head,,TRIzol Invitrogen extraction per manufactor's instructions Strand specific  polyA selected RNA Seq libraries were constructed using a custom dUTP method similar to the standard Illumina protocols  with the addition of 1ul of a 1:10 dilution of ERCC RNA spike ins prior to polyA selection.,Zebrafish embryos from natural matings were maintained at 28C in 6 or 10cm dishes. 5 dpf  the heads of 80 100 embryos per replicate were obtained for RNA extraction.,develolpmental stage:5 dpf embryo|tissue:whole head,GSM1543672,GSM1543672: Wildtype Replicate 1; Danio rerio; RNA Seq,GSM1543672,,1,TRIzol Invitrogen extraction per manufactor's instructions Strand specific  polyA selected RNA Seq libraries were constructed using a custom dUTP method similar to the standard Illumina protocols  with the addition of 1ul of a 1:10 dilution of ERCC RNA spike ins prior to polyA selection.,GEO Accession:GSM1543672,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2000,,SRP049716,,,uninjected_rep1_zebrafish_121230_AC1BMGACXX_Illumina2_1.fastq.gz uninjected_rep1_zebrafish_121230_AC1BMGACXX_Illumina2_2.fastq.gz,fastq fastq,5994627800.0,59946278.0,GSM1543672 r1,0:50 1:50,A:1649718236;C:1309696705;G:1340401079;T:1694576298;N:235482,50,50,,,1649718236,1309696705,1340401079,1694576298,235482,SRX757981,SRS743128,SRA200859,GEO,"Center for Human Genetic Research, Massachusetts General Hospital",2,0.9191,0.92223,0.18431,0.18241,0.68889,0.68793,0.48942,0.48534,50,50,B,B,biological fallback assumption,illumina,hiseq_era,unknown,poly_a,unknown,bulk,unknown,unknown,,United States,2014-11-12,Larval,Larval,Head,Nervous System
39887,SRR2239197,SRX1181673,SRS1053962,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,mutant 5 hr treatment replicate 3,GSM1868446,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:metronidazole|time:5 hr|tissue:head,mutant 5 hr treatment replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:metronidazole|time:5 hr|tissue:head,GSM1868446,GSM1868446: mutant 5 hr treatment replicate 3; Danio rerio; RNA Seq,GSM1868446,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868446,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1349_s_3_withindex_sequence.txt_AGGCGAA.fq.gz,fastq,1486758800.0,29735176.0,GSM1868446 r1,0:50,A:407157206;C:348516474;G:333581236;T:397373823;N:130061,50,,,,407157206,348516474,333581236,397373823,130061,SRX1181673,SRS1053962,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89356,,0.24716,,0.66348,,0.55072,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39888,SRR2239196,SRX1181672,SRS1053963,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,mutant 5 hr treatment replicate 2,GSM1868445,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:metronidazole|time:5 hr|tissue:head,mutant 5 hr treatment replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:metronidazole|time:5 hr|tissue:head,GSM1868445,GSM1868445: mutant 5 hr treatment replicate 2; Danio rerio; RNA Seq,GSM1868445,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868445,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1349_s_3_withindex_sequence.txt_AATTCAT.fq.gz,fastq,1324305100.0,26486102.0,GSM1868445 r1,0:50,A:346866338;C:322967018;G:303987755;T:350367920;N:116069,50,,,,346866338,322967018,303987755,350367920,116069,SRX1181672,SRS1053963,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.86992,,0.2794,,0.67087,,0.45,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39889,SRR2239195,SRX1181671,SRS1053965,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,mutant 5 hr treatment replicate 1,GSM1868444,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:metronidazole|time:5 hr|tissue:head,mutant 5 hr treatment replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:metronidazole|time:5 hr|tissue:head,GSM1868444,GSM1868444: mutant 5 hr treatment replicate 1; Danio rerio; RNA Seq,GSM1868444,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868444,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1349_s_3_withindex_sequence.txt_CTGCAAT.fq.gz,fastq,1996223000.0,39924460.0,GSM1868444 r1,0:50,A:548376523;C:462971670;G:439194387;T:545504649;N:175771,50,,,,548376523,462971670,439194387,545504649,175771,SRX1181671,SRS1053965,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.90072,,0.27661,,0.66809,,0.54999,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39890,SRR2239194,SRX1181670,SRS1053966,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,mutant control replicate 3,GSM1868443,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:control|tissue:head,mutant control replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:control|tissue:head,GSM1868443,GSM1868443: mutant control replicate 3; Danio rerio; RNA Seq,GSM1868443,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868443,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1349_s_3_withindex_sequence.txt_GTAAAAA.fq.gz,fastq,1689695100.0,33793902.0,GSM1868443 r1,0:50,A:469281850;C:387188418;G:368970934;T:464103273;N:150625,50,,,,469281850,387188418,368970934,464103273,150625,SRX1181670,SRS1053966,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.88353,,0.30543,,0.66785,,0.53952,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39891,SRR2239193,SRX1181669,SRS1053964,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,mutant control replicate 2,GSM1868442,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:control|tissue:head,mutant control replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:control|tissue:head,GSM1868442,GSM1868442: mutant control replicate 2; Danio rerio; RNA Seq,GSM1868442,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868442,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1349_s_3_withindex_sequence.txt_TGGCATA.fq.gz,fastq,1744754500.0,34895090.0,GSM1868442 r1,0:50,A:475432211;C:407457752;G:387941759;T:473768506;N:154272,50,,,,475432211,407457752,387941759,473768506,154272,SRX1181669,SRS1053964,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.8967,,0.27571,,0.66342,,0.5413,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39892,SRR2239192,SRX1181668,SRS1053967,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,mutant control replicate 1,GSM1868441,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:control|tissue:head,mutant control replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:foxd3 / |agent:control|tissue:head,GSM1868441,GSM1868441: mutant control replicate 1; Danio rerio; RNA Seq,GSM1868441,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868441,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1349_s_3_withindex_sequence.txt_GGAGTCC.fq.gz,fastq,1300091300.0,26001826.0,GSM1868441 r1,0:50,A:356312292;C:301731841;G:287159447;T:354773803;N:113917,50,,,,356312292,301731841,287159447,354773803,113917,SRX1181668,SRS1053967,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89407,,0.27485,,0.66263,,0.54402,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39893,SRR2239190,SRX1181667,SRS1053968,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 5 hr treatment replicate 3,GSM1868440,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,wild type 5 hr treatment replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,GSM1868440,GSM1868440: wild type 5 hr treatment replicate 3; Danio rerio; RNA Seq,GSM1868440,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868440,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_GGTCCTC.fq.gz,fastq,788127550.0,15762551.0,GSM1868440 r1,0:50,A:219123307;C:174342061;G:168810140;T:225814483;N:37559,50,,,,219123307,174342061,168810140,225814483,37559,SRX1181667,SRS1053968,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89391,,0.27826,,0.67034,,0.55775,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39894,SRR2239191,SRX1181667,SRS1053968,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 5 hr treatment replicate 3,GSM1868440,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,wild type 5 hr treatment replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,GSM1868440,GSM1868440: wild type 5 hr treatment replicate 3; Danio rerio; RNA Seq,GSM1868440,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868440,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_GGTCCTC.fq.gz,fastq,779058950.0,15581179.0,GSM1868440 r2,0:50,A:216843690;C:172197112;G:166801096;T:223172377;N:44675,50,,,,216843690,172197112,166801096,223172377,44675,SRX1181667,SRS1053968,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89268,,0.27974,,0.67067,,0.55617,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39895,SRR2239188,SRX1181666,SRS1053969,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 5 hr treatment replicate 2,GSM1868439,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,wild type 5 hr treatment replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,GSM1868439,GSM1868439: wild type 5 hr treatment replicate 2; Danio rerio; RNA Seq,GSM1868439,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868439,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_GCTTAGA.fq.gz,fastq,884810450.0,17696209.0,GSM1868439 r1,0:50,A:244801024;C:196884736;G:189692109;T:253390454;N:42127,50,,,,244801024,196884736,189692109,253390454,42127,SRX1181666,SRS1053969,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89625,,0.26571,,0.66247,,0.52896,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39896,SRR2239189,SRX1181666,SRS1053969,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 5 hr treatment replicate 2,GSM1868439,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,wild type 5 hr treatment replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,GSM1868439,GSM1868439: wild type 5 hr treatment replicate 2; Danio rerio; RNA Seq,GSM1868439,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868439,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_GCTTAGA.fq.gz,fastq,875476350.0,17509527.0,GSM1868439 r2,0:50,A:242411986;C:194719083;G:187698234;T:250595738;N:51309,50,,,,242411986,194719083,187698234,250595738,51309,SRX1181666,SRS1053969,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89632,,0.26574,,0.66332,,0.53633,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39897,SRR2239186,SRX1181665,SRS1053970,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 5 hr treatment replicate 1,GSM1868438,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,wild type 5 hr treatment replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,GSM1868438,GSM1868438: wild type 5 hr treatment replicate 1; Danio rerio; RNA Seq,GSM1868438,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868438,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_GTCGATA.fq.gz,fastq,981479900.0,19629598.0,GSM1868438 r1,0:50,A:272447863;C:217586061;G:210457740;T:280941539;N:46697,50,,,,272447863,217586061,210457740,280941539,46697,SRX1181665,SRS1053970,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89259,,0.28519,,0.66413,,0.54434,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39898,SRR2239187,SRX1181665,SRS1053970,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 5 hr treatment replicate 1,GSM1868438,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,wild type 5 hr treatment replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:5 hr|tissue:head,GSM1868438,GSM1868438: wild type 5 hr treatment replicate 1; Danio rerio; RNA Seq,GSM1868438,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868438,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_GTCGATA.fq.gz,fastq,970627300.0,19412546.0,GSM1868438 r2,0:50,A:269587370;C:215107358;G:208077535;T:277799059;N:55978,50,,,,269587370,215107358,208077535,277799059,55978,SRX1181665,SRS1053970,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.8924,,0.2863,,0.66486,,0.54277,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39899,SRR2239184,SRX1181664,SRS1053971,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 2 hr treatment replicate 3,GSM1868437,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,wild type 2 hr treatment replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,GSM1868437,GSM1868437: wild type 2 hr treatment replicate 3; Danio rerio; RNA Seq,GSM1868437,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868437,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_AGATACT.fq.gz,fastq,1034107450.0,20682149.0,GSM1868437 r1,0:50,A:263807622;C:250451504;G:242163638;T:277636652;N:48034,50,,,,263807622,250451504,242163638,277636652,48034,SRX1181664,SRS1053971,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.90878,,0.23218,,0.65916,,0.49411,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39900,SRR2239185,SRX1181664,SRS1053971,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 2 hr treatment replicate 3,GSM1868437,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,wild type 2 hr treatment replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,GSM1868437,GSM1868437: wild type 2 hr treatment replicate 3; Danio rerio; RNA Seq,GSM1868437,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868437,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_AGATACT.fq.gz,fastq,1021705150.0,20434103.0,GSM1868437 r2,0:50,A:260838269;C:247381617;G:239188036;T:274238961;N:58267,50,,,,260838269,247381617,239188036,274238961,58267,SRX1181664,SRS1053971,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.91116,,0.23255,,0.65918,,0.49596,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39901,SRR2239182,SRX1181663,SRS1053972,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 2 hr treatment replicate 2,GSM1868436,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,wild type 2 hr treatment replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,GSM1868436,GSM1868436: wild type 2 hr treatment replicate 2; Danio rerio; RNA Seq,GSM1868436,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868436,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_GGGTCAA.fq.gz,fastq,756008650.0,15120173.0,GSM1868436 r1,0:50,A:209261412;C:168123618;G:163450516;T:215134424;N:38680,50,,,,209261412,168123618,163450516,215134424,38680,SRX1181663,SRS1053972,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.8978,,0.26699,,0.66172,,0.53653,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39902,SRR2239183,SRX1181663,SRS1053972,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 2 hr treatment replicate 2,GSM1868436,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,wild type 2 hr treatment replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,GSM1868436,GSM1868436: wild type 2 hr treatment replicate 2; Danio rerio; RNA Seq,GSM1868436,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868436,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_GGGTCAA.fq.gz,fastq,747959000.0,14959180.0,GSM1868436 r2,0:50,A:207110574;C:166254650;G:161670187;T:212878047;N:45542,50,,,,207110574,166254650,161670187,212878047,45542,SRX1181663,SRS1053972,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89508,,0.26657,,0.66373,,0.53734,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39903,SRR2239180,SRX1181662,SRS1053973,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 2 hr treatment replicate 1,GSM1868435,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,wild type 2 hr treatment replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,GSM1868435,GSM1868435: wild type 2 hr treatment replicate 1; Danio rerio; RNA Seq,GSM1868435,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868435,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_CAATATC.fq.gz,fastq,843938700.0,16878774.0,GSM1868435 r1,0:50,A:235353785;C:185755129;G:180220044;T:242567413;N:42329,50,,,,235353785,185755129,180220044,242567413,42329,SRX1181662,SRS1053973,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.8819,,0.31587,,0.6719,,0.53852,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39904,SRR2239181,SRX1181662,SRS1053973,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type 2 hr treatment replicate 1,GSM1868435,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,wild type 2 hr treatment replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:metronidazole|time:2 hr|tissue:head,GSM1868435,GSM1868435: wild type 2 hr treatment replicate 1; Danio rerio; RNA Seq,GSM1868435,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868435,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_CAATATC.fq.gz,fastq,837375500.0,16747510.0,GSM1868435 r2,0:50,A:233691274;C:184249473;G:178762050;T:240622009;N:50694,50,,,,233691274,184249473,178762050,240622009,50694,SRX1181662,SRS1053973,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.88228,,0.31306,,0.67042,,0.53933,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39905,SRR2239178,SRX1181661,SRS1053976,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type control replicate 3,GSM1868434,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,wild type control replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,GSM1868434,GSM1868434: wild type control replicate 3; Danio rerio; RNA Seq,GSM1868434,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868434,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_ACCCACT.fq.gz,fastq,946427500.0,18928550.0,GSM1868434 r1,0:50,A:260851494;C:211313068;G:205344403;T:268874280;N:44255,50,,,,260851494,211313068,205344403,268874280,44255,SRX1181661,SRS1053976,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89626,,0.27082,,0.66058,,0.53343,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39906,SRR2239179,SRX1181661,SRS1053976,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type control replicate 3,GSM1868434,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,wild type control replicate 3,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,GSM1868434,GSM1868434: wild type control replicate 3; Danio rerio; RNA Seq,GSM1868434,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868434,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_ACCCACT.fq.gz,fastq,935318450.0,18706369.0,GSM1868434 r2,0:50,A:258004973;C:208706255;G:202911059;T:265642847;N:53316,50,,,,258004973,208706255,202911059,265642847,53316,SRX1181661,SRS1053976,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89576,,0.27216,,0.663,,0.53587,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39907,SRR2239176,SRX1181660,SRS1053974,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type control replicate 2,GSM1868433,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,wild type control replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,GSM1868433,GSM1868433: wild type control replicate 2; Danio rerio; RNA Seq,GSM1868433,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868433,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_TCAACTG.fq.gz,fastq,914021500.0,18280430.0,GSM1868433 r1,0:50,A:252009242;C:204125475;G:197760562;T:260083313;N:42908,50,,,,252009242,204125475,197760562,260083313,42908,SRX1181660,SRS1053974,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89646,,0.26998,,0.65979,,0.53202,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39908,SRR2239177,SRX1181660,SRS1053974,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type control replicate 2,GSM1868433,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,wild type control replicate 2,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,GSM1868433,GSM1868433: wild type control replicate 2; Danio rerio; RNA Seq,GSM1868433,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868433,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_TCAACTG.fq.gz,fastq,904836300.0,18096726.0,GSM1868433 r2,0:50,A:249726925;C:201939252;G:195727802;T:257389594;N:52727,50,,,,249726925,201939252,195727802,257389594,52727,SRX1181660,SRS1053974,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89504,,0.27105,,0.6607,,0.5314,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39909,SRR2239174,SRX1181659,SRS1053975,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type control replicate 1,GSM1868432,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,wild type control replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,GSM1868432,GSM1868432: wild type control replicate 1; Danio rerio; RNA Seq,GSM1868432,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868432,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_6_withindex_sequence.txt_TTTAACT.fq.gz,fastq,919147800.0,18382956.0,GSM1868432 r1,0:50,A:255238211;C:203629686;G:197780664;T:262454873;N:44366,50,,,,255238211,203629686,197780664,262454873,44366,SRX1181659,SRS1053975,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89498,,0.2793,,0.6636,,0.54563,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
39910,SRR2239175,SRX1181659,SRS1053975,SRP063290,PRJNA294660,Transcriptome analysis of metronidazole induced sensory neuron ablation in zebrafish,GSE72682,Transcriptome Analysis,Damage to and/or loss of sensory neurons can result in debilitating neuropathies that often have a dramatic impact on quality of life. The cellular mechanisms involved in the response of neurons and glia to such pathological insults are poorly understood. Investigation has shown that peripheral glia play critical roles in both the degenerative and regenerative processes that are involved in the responses to peripheral nerve damage. The vast majority of studies have focused primarily on myelinating Schwann cells]  with the result that very little is known regarding how the non myelinating glia that ensheath axons and neuronal somas respond to nerve damage. This is a significant knowledge gap  given that over 80% of cutaneous fibers are unmyelinated  that they transduce such important modalities as itch  pain  temperature  touch and pressure  and that they are affected in many prevalent peripheral neuropathies. It is the goal of this study to shed light on the genetic programs involved in the responses of non myelinating glia roles to nerve degeneration. We utilized RNA seq to identify genes that were differentially expressed in the larval head during the process of sensory neuron ablation and axon degeneration in both wild type larvae and in larvae that do not have peripheral glia foxd3 mutants using a selective  conditional approach. Overall  the information regarding differential gene expression in these conditions will provide a basis for further investigation into the cellular processes that underlie pathophysiological responses of neurons and glia to sensory nerve damage. Overall design: mRNA levels were determined using biological triplicate samples from five sets of samples. Three sets from wild type: control  2 hrs of metronidazole treatment and 5 hrs of metronidazole treatment. And two sets from foxd3 mutants: control and 5hrs of metronidazole treatment.,,pubmed:26863206,,wild type control replicate 1,GSM1868432,,source name:head|age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,wild type control replicate 1,Read alignment used STAR ver 2.0.04b Gene counts were derived from the number of uniquely aligned unambiguous reads by Subread:featureCount version 1.4.5. Transcript counts were produced by Sailfish version 0.6.3. Sequencing performance was assessed for total number of aligned reads  total number of uniquely aligned reads  genes and transcripts detected  ribosomal fraction  known junction saturation and read distribution over known gene models with RSeQC version 2.3. All gene level and transcript counts were imported into the R/Bioconductor package EdgeR and TMM normalized to adjust for differences in library size. Generalized linear models with robust dispersion estimates were created to test for gene/transcript level differential expression. The fit of the trended and tagwise dispersion estimates were then plotted to confirm proper fit of the observed mean to variance relationship where the tagwise dispersions are equivalent to the biological coefficients of variation of each gene. Differentially expressed genes and transcripts were then filtered for those having fold changes FC > 1.2 together with false discovery rate FDR adjusted p values less than or equal to 0.05. R/Bioconductor package “gplots” was used to generate heatmaps. The differentially expressed zebrafish genes in each condition were transferred to their human orthology by using the PANTHER classification system http://pantherdb.org/genes/index.jsp  then GO enrichment analysis was performed in ToppGene suite  with the p value cut off < 0.05 B&H corrected. Genome build: Danio rerio Zv9 assembly from Ensembl Supplementary files format and content: wt.txt and mutant.txt report gene counts RPKMs,head,For treated samples  4 dpf larvae were exposed to 10 mM metronidazole in fish water for either 2 hrs or 5 hrs.,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,,age:4 dpf|developmental stage:larvae|genotype/variation:AB wild type|agent:control|tissue:head,GSM1868432,GSM1868432: wild type control replicate 1; Danio rerio; RNA Seq,GSM1868432,,1,Heads of 4 dpf larvae exposed to 10 mM MET for either 0  2 or 5 hours were dissected using a small scalpel  with 8 heads pooled per sample. Each sample was then homogenized in 250 mL of TRIzol Life Technologies  and total RNA extracted. The RNA samples were then treated with DNase and column purified using a Qiagen RNEasy mini kit Qiagen  Inc.. Biological triplicates 8 heads per replicate were prepared for each condition. RNA purity and integrity was determined using an Agilent Bioanalyzer 2100  and only those samples having a RIN > 8.7 were used. For library construction  1 μg total RNA was used for each wild type replicate and 0.35 μg for the mutant replicates. The total RNA samples were depleted of rRNA using the Ribo Zero protocol Epicentre. cDNA was synthesized  blunt ended  an A base added to the 3’ ends and then had Illumina sequencing adapters ligated. cDNA fragments were then amplified for 12 cycles using primers incorporating unique index tags.,GEO Accession:GSM1868432,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2500,,SRP063290,,,run_1266_s_7_withindex_sequence.txt_TTTAACT.fq.gz,fastq,908786950.0,18175739.0,GSM1868432 r2,0:50,A:252518589;C:201251252;G:195514386;T:259449857;N:52866,50,,,,252518589,201251252,195514386,259449857,52866,SRX1181659,SRS1053975,SRA294351,GEO,"Voigt, Pharmacology and Physiology, Saint Louis University",1,0.89351,,0.27857,,0.66492,,0.54418,,50,,B,,usable mapping rate,illumina,hiseq_era,unknown,poly_a,ribozero,bulk,unknown,unknown,,United States,2015-09-03,Larval,Larval,Head,Nervous System
40494,SRR3204724,SRX1614066,SRS1323928,SRP070923,PRJNA313387,Transcriptomic of ß diketone antibiotics on zebrafish post a 3 month DKAs exposure.,PRJNA313387,Other,RNA libraries were constructed from control  6.25 and 12.5 mg/L treatment groups  respectively. post DKAs exposure to 3 mpf zebrafish  the whole transcriptome was determined.,,,12.5 mg/L with equal weight concentrations and volumes for each of the six DKA species ofloxacin  ciprofloxacin  enrofloxacin  doxycycline  chlortetracycline and oxytetracycline was exposure to zebrafish from embryo to 90 dpf dpf,12.5mg/L DKAs,T21,,strain:AB strain|isolate:Oregon State University|breed:Danio rerio|cultivar:not applicable|ecotype:Wild type|age:3 mpf|dev stage:3 mpf|sex:pooled male and female|tissue:we performed simple anatomy of the whole fish  i.e. removing gill  fin and tail tissue  while retaining visceral mass  head  spine and other nerve systems.|treatment:12.5 mg/L DKAs exposure|BioSampleModel:Model organism or animal,,,,,,,,,12.5mg/L DKAs,T21,1,Zebrafish in 12.5 mg/L β diketone antibiotics  treatment groupwith equal weight concentrations and volumes for ofloxacin  ciprofloxacin  enrofloxacin  doxycycline  chlortetracycline and oxytetracycline with purity of 99% except for 95% for chlortetracycline were randomly selected post DKAs exposure at 90 dpf  and rinsed with phosphorous buffer solution. We performed simple anatomy of the whole fish  i.e.  removing gill  fin and tail tissue  while retaining visceral mass  head  spine and other nerve systems. The retained tissues were used to extract total RNA  using Trizol Invitrogen  Carlsbad  CA  USA according to the manufacturer's procedures. The quantity and purity of total RNA were analyzed by employing a Bioanalyzer 2100 and RNA 6000 Nano LabChipKit Agilent  Santa Clara  CA  USA with RIN number >7.0. Poly A mRNA was isolated by poly T oligo attached magnetic beads Invitrogen. The purified mRNA was fragmented into small pieces by divalent cations under elevated temperature. Then the final cDNA library was produced by the reverse transcription of the cleaved RNA fragments on the basis of the mRNA Seq sample preparation kit Illumina  San Diego  USA  and the average 300±50 bp insert size was used for the paired end libraries. Finally  the paired end sequencing was performed on an Illumina Hiseq2000/2500.    Prior to assembly  the low quality reads 1  reads containing sequencing adaptors; 2  reads containing sequencing primer; 3  nucleotide with q scores lower than 20 were removed. Next  the cleaned and paired end reads were produced.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2500,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>200</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC><READ_SPEC><READ_INDEX>1</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Reverse</READ_TYPE><BASE_COORD>101</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP070923,,,T21_Clean_Data1.fq.gz T21_Clean_Data2.fq.gz,fastq fastq,10502615500.0,42010462.0,T21,0:125 1:125,A:2848309151;C:2371408734;G:2356749579;T:2925931092;N:216944,125,125,,,2848309151,2371408734,2356749579,2925931092,216944,SRX1614066,SRS1323928,SRA359545,School of Life Sciences,School of Life Sciences,2,0.87768,0.88612,0.29688,0.29743,0.68738,0.68363,0.52932,0.52507,125,125,B,B,biological fallback assumption,illumina,hiseq_era,full_length,poly_a,unknown,bulk,unknown,unknown,,Unknown,2016-03-16,Adult,Adult,Head,Nervous System
40495,SRR3203073,SRX1612569,SRS1321766,SRP070923,PRJNA313387,Transcriptomic of ß diketone antibiotics on zebrafish post a 3 month DKAs exposure.,PRJNA313387,Other,RNA libraries were constructed from control  6.25 and 12.5 mg/L treatment groups  respectively. post DKAs exposure to 3 mpf zebrafish  the whole transcriptome was determined.,,,6.25 mg/L with equal weight concentrations and volumes for each of the six DKA species ofloxacin  ciprofloxacin  enrofloxacin  doxycycline  chlortetracycline and oxytetracycline was exposure to zebrafish from embryo to 90 dpf dpf,6.25mg/L DKAs,T11,,strain:AB strain|isolate:Oregon State University|breed:Danio rerio|cultivar:not applicable|ecotype:Wild type|age:3 mpf|dev stage:3 mpf|sex:pooled male and female|tissue:we performed simple anatomy of the whole fish  i.e. removing gill  fin and tail tissue  while retaining visceral mass  head  spine and other nerve systems.|treatment:6.25 mg/L DKAs exposure|BioSampleModel:Model organism or animal,,,,,,,,,6.25 mg/L DKAs,T11,1,Zebrafish in 6.25 mg/L β diketone antibiotics  treatment groupwith equal weight concentrations and volumes for ofloxacin  ciprofloxacin  enrofloxacin  doxycycline  chlortetracycline and oxytetracycline with purity of 99% except for 95% for chlortetracycline were randomly selected post DKAs exposure at 90 dpf  and rinsed with phosphorous buffer solution. We performed simple anatomy of the whole fish  i.e.  removing gill  fin and tail tissue  while retaining visceral mass  head  spine and other nerve systems. The retained tissues were used to extract total RNA  using Trizol Invitrogen  Carlsbad  CA  USA according to the manufacturer's procedures. The quantity and purity of total RNA were analyzed by employing a Bioanalyzer 2100 and RNA 6000 Nano LabChipKit Agilent  Santa Clara  CA  USA with RIN number >7.0. Poly A mRNA was isolated by poly T oligo attached magnetic beads Invitrogen. The purified mRNA was fragmented into small pieces by divalent cations under elevated temperature. Then the final cDNA library was produced by the reverse transcription of the cleaved RNA fragments on the basis of the mRNA Seq sample preparation kit Illumina  San Diego  USA  and the average 300±50 bp insert size was used for the paired end libraries. Finally  the paired end sequencing was performed on an Illumina Hiseq2000/2500.    Prior to assembly  the low quality reads 1  reads containing sequencing adaptors; 2  reads containing sequencing primer; 3  nucleotide with q scores lower than 20 were removed. Next  the cleaned and paired end reads were produced.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2500,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>200</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC><READ_SPEC><READ_INDEX>1</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Reverse</READ_TYPE><BASE_COORD>101</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP070923,,,T11_Clean_Data1.fq.gz T11_Clean_Data2.fq.gz,fastq fastq,8178356500.0,32713426.0,T11,0:125 1:125,A:2135090304;C:1929011381;G:1912585084;T:2201518295;N:151436,125,125,,,2135090304,1929011381,1912585084,2201518295,151436,SRX1612569,SRS1321766,SRA359545,School of Life Sciences,School of Life Sciences,2,0.84003,0.84827,0.32283,0.32402,0.71031,0.70502,0.58398,0.58631,125,125,B,B,biological fallback assumption,illumina,hiseq_era,full_length,poly_a,unknown,bulk,unknown,unknown,,Unknown,2016-03-15,Adult,Adult,Head,Nervous System
40496,SRR3195594,SRX1604653,SRS1314385,SRP070923,PRJNA313387,Transcriptomic of ß diketone antibiotics on zebrafish post a 3 month DKAs exposure.,PRJNA313387,Other,RNA libraries were constructed from control  6.25 and 12.5 mg/L treatment groups  respectively. post DKAs exposure to 3 mpf zebrafish  the whole transcriptome was determined.,,,,,zebrafish,,strain:AB strain|isolate:Oregon State University|breed:Danio rerio|cultivar:not applicable|ecotype:Wild type|age:3 mpf|dev stage:3 mpf|sex:pooled male and female|tissue:we performed simple anatomy of the whole fish  i.e.  removing gill  fin and tail tissue  while retaining visceral mass  head  spine and other nerve systems.|BioSampleModel:Model organism or animal,,,,,,,,,control,CON 01,1,Zebrafish in control group were randomly selected post DKAs exposure at 90 dpf  and rinsed with phosphorous buffer solution. We performed simple anatomy of the whole fish  i.e.  removing gill  fin and tail tissue  while retaining visceral mass  head  spine and other nerve systems. The retained tissues were used to extract total RNA according to the manufacturer's procedures. The quantity and purity of total RNA were analyzed by employing a Bioanalyzer 2100 and RNA 6000 Nano LabChipKit Agilent  Santa Clara  CA  USA with RIN number >7.0. Poly A mRNA was isolated by poly T oligo attached magnetic beads Invitrogen. The purified mRNA was fragmented into small pieces by divalent cations under elevated temperature. Then the final cDNA library was produced by the reverse transcription of the cleaved RNA fragments on the basis of the mRNA Seq sample preparation kit Illumina  San Diego  USA  and the average 300±50 bp insert size was used for the paired end libraries. Finally  the paired end sequencing was performed on an Illumina Hiseq2000/2500.    Prior to assembly  the low quality reads 1  reads containing sequencing adaptors; 2  reads containing sequencing primer; 3  nucleotide with q scores lower than 20 were removed. Next  the cleaned and paired end reads were produced.,,,RNA-Seq,TRANSCRIPTOMIC,cDNA,PAIRED,ILLUMINA,Illumina HiSeq 2500,<SPOT_DESCRIPTOR><SPOT_DECODE_SPEC><SPOT_LENGTH>200</SPOT_LENGTH><READ_SPEC><READ_INDEX>0</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Forward</READ_TYPE><BASE_COORD>1</BASE_COORD></READ_SPEC><READ_SPEC><READ_INDEX>1</READ_INDEX><READ_CLASS>Application Read</READ_CLASS><READ_TYPE>Reverse</READ_TYPE><BASE_COORD>101</BASE_COORD></READ_SPEC></SPOT_DECODE_SPEC></SPOT_DESCRIPTOR>,SRP070923,,,CON_01_Clean_Data2.fq.gz CON_01_Clean_Data1.fq.gz,fastq fastq,8941582750.0,35766331.0,control,0:125 1:125,A:2282842470;C:2172817074;G:2169521320;T:2316254609;N:147277,125,125,,,2282842470,2172817074,2169521320,2316254609,147277,SRX1604653,SRS1314385,SRA359545,School of Life Sciences,School of Life Sciences,2,0.62865,0.62758,0.22408,0.21961,0.7525,0.75024,0.5332,0.519,125,125,B,B,biological fallback assumption,illumina,hiseq_era,full_length,poly_a,unknown,bulk,unknown,unknown,,Unknown,2016-03-15,Adult,Adult,Head,Nervous System
41655,SRR5115728,SRX2431099,SRS1866976,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,18 hpi rep5,GSM2430667,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,18 hpi rep5,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,GSM2430667,GSM2430667: 18 hpi rep5; Danio rerio; RNA Seq,GSM2430667,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430667,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,18hpi_54366.fastq.gz,fastq,3043532908.0,58529479.0,GSM2430667 r1,0:52,A:729034781;C:769509924;G:743085356;T:801831768;N:71079,52,,,,729034781,769509924,743085356,801831768,71079,SRX2431099,SRS1866976,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.73906,,0.22225,,0.74061,,0.49988,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41656,SRR5115727,SRX2431098,SRS1866975,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,18 hpi rep4,GSM2430666,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,18 hpi rep4,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,GSM2430666,GSM2430666: 18 hpi rep4; Danio rerio; RNA Seq,GSM2430666,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430666,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,18hpi_48592.fastq.gz,fastq,2622132240.0,50425620.0,GSM2430666 r1,0:52,A:566371236;C:777180578;G:659521124;T:618999154;N:60148,52,,,,566371236,777180578,659521124,618999154,60148,SRX2431098,SRS1866975,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.92057,,0.28475,,0.86833,,0.72823,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41657,SRR5115726,SRX2431097,SRS1866974,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,18 hpi rep3,GSM2430665,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,18 hpi rep3,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,GSM2430665,GSM2430665: 18 hpi rep3; Danio rerio; RNA Seq,GSM2430665,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430665,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,18hpi_48591.fastq.gz,fastq,2478119176.0,47656138.0,GSM2430665 r1,0:52,A:493736890;C:768557459;G:661870968;T:553896608;N:57251,52,,,,493736890,768557459,661870968,553896608,57251,SRX2431097,SRS1866974,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.96537,,0.26164,,0.87892,,0.7204,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41658,SRR5115725,SRX2431096,SRS1866973,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,18 hpi rep2,GSM2430664,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,18 hpi rep2,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,GSM2430664,GSM2430664: 18 hpi rep2; Danio rerio; RNA Seq,GSM2430664,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430664,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,18hpi_48590.fastq.gz,fastq,2414695452.0,46436451.0,GSM2430664 r1,0:52,A:475090050;C:755838280;G:657771658;T:525939134;N:56330,52,,,,475090050,755838280,657771658,525939134,56330,SRX2431096,SRS1866973,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.9654,,0.26982,,0.89676,,0.72161,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41659,SRR5115724,SRX2431095,SRS1866972,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,18 hpi rep1,GSM2430663,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,18 hpi rep1,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:18,GSM2430663,GSM2430663: 18 hpi rep1; Danio rerio; RNA Seq,GSM2430663,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430663,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,18hpi_48589.fastq.gz,fastq,2275983060.0,43768905.0,GSM2430663 r1,0:52,A:466133336;C:694614756;G:598071579;T:517110546;N:52843,52,,,,466133336,694614756,598071579,517110546,52843,SRX2431095,SRS1866972,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.94909,,0.2695,,0.86809,,0.70019,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41660,SRR5115723,SRX2431094,SRS1866971,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,9 hpi rep5,GSM2430662,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,9 hpi rep5,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,GSM2430662,GSM2430662: 9 hpi rep5; Danio rerio; RNA Seq,GSM2430662,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430662,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,9hpi_54368.fastq.gz,fastq,2831111348.0,54444449.0,GSM2430662 r1,0:52,A:674270099;C:713818041;G:694997603;T:747958840;N:66765,52,,,,674270099,713818041,694997603,747958840,66765,SRX2431094,SRS1866971,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.81449,,0.24117,,0.74091,,0.53961,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41661,SRR5115722,SRX2431093,SRS1866970,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,9 hpi rep4,GSM2430661,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,9 hpi rep4,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,GSM2430661,GSM2430661: 9 hpi rep4; Danio rerio; RNA Seq,GSM2430661,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430661,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,9hpi_48586.fastq.gz,fastq,3247890880.0,62459440.0,GSM2430661 r1,0:52,A:737775958;C:866361850;G:806031275;T:837644754;N:77043,52,,,,737775958,866361850,806031275,837644754,77043,SRX2431093,SRS1866970,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.88824,,0.26531,,0.77619,,0.64707,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41662,SRR5115721,SRX2431092,SRS1866969,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,9 hpi rep3,GSM2430660,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,9 hpi rep3,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,GSM2430660,GSM2430660: 9 hpi rep3; Danio rerio; RNA Seq,GSM2430660,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430660,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,9hpi_48585.fastq.gz,fastq,2383588948.0,45838249.0,GSM2430660 r1,0:52,A:471509922;C:736118462;G:639172021;T:536732824;N:55719,52,,,,471509922,736118462,639172021,536732824,55719,SRX2431092,SRS1866969,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.96831,,0.25406,,0.88327,,0.69186,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41663,SRR5115720,SRX2431091,SRS1866968,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,9 hpi rep2,GSM2430659,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,9 hpi rep2,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,GSM2430659,GSM2430659: 9 hpi rep2; Danio rerio; RNA Seq,GSM2430659,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430659,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,9hpi_48584.fastq.gz,fastq,2858494184.0,54971042.0,GSM2430659 r1,0:52,A:601123087;C:841668883;G:744364922;T:671270980;N:66312,52,,,,601123087,841668883,744364922,671270980,66312,SRX2431091,SRS1866968,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.93531,,0.28407,,0.86277,,0.73297,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41664,SRR5115719,SRX2431090,SRS1866967,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,9 hpi rep1,GSM2430658,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,9 hpi rep1,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:9,GSM2430658,GSM2430658: 9 hpi rep1; Danio rerio; RNA Seq,GSM2430658,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430658,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,9hpi_48583.fastq.gz,fastq,2348023808.0,45154304.0,GSM2430658 r1,0:52,A:520788777;C:655035758;G:589264364;T:582879912;N:54997,52,,,,520788777,655035758,589264364,582879912,54997,SRX2431090,SRS1866967,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.90637,,0.26958,,0.80649,,0.68165,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41665,SRR5115718,SRX2431089,SRS1866966,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,0 hpi rep4,GSM2430657,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,0 hpi rep4,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,GSM2430657,GSM2430657: 0 hpi rep4; Danio rerio; RNA Seq,GSM2430657,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430657,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,0hpi_54367.fastq.gz,fastq,3737365060.0,71872405.0,GSM2430657 r1,0:52,A:898855616;C:929504130;G:883445728;T:1025471492;N:88094,52,,,,898855616,929504130,883445728,1025471492,88094,SRX2431089,SRS1866966,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.80824,,0.21971,,0.75511,,0.45635,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41666,SRR5115717,SRX2431088,SRS1866965,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,0 hpi rep3,GSM2430656,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,0 hpi rep3,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,GSM2430656,GSM2430656: 0 hpi rep3; Danio rerio; RNA Seq,GSM2430656,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430656,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,0hpi_54365.fastq.gz,fastq,2479423440.0,47681220.0,GSM2430656 r1,0:52,A:585035619;C:641794408;G:600148220;T:652388942;N:56251,52,,,,585035619,641794408,600148220,652388942,56251,SRX2431088,SRS1866965,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.7459,,0.20704,,0.76674,,0.44617,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41667,SRR5115716,SRX2431087,SRS1866964,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,0 hpi rep2,GSM2430655,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,0 hpi rep2,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,GSM2430655,GSM2430655: 0 hpi rep2; Danio rerio; RNA Seq,GSM2430655,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430655,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,0hpi_48587.fastq.gz,fastq,2251744196.0,43302773.0,GSM2430655 r1,0:52,A:446930339;C:692500195;G:602614693;T:509646110;N:52859,52,,,,446930339,692500195,602614693,509646110,52859,SRX2431087,SRS1866964,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.96295,,0.25309,,0.90035,,0.717,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System
41668,SRR5115715,SRX2431086,SRS1866963,SRP095238,PRJNA357683,Transcriptome and Functional Analyses Reveal Roles For Regulators of Epigenetic States  Micro RNA Processing  And Long Non Coding RNA In Myocyte Dedifferentiation: Insights Into Reprogramming A “Post Mitotic” Cell,GSE92489,Transcriptome Analysis,Purpose: The ability of adult zebrafish tissues to undergo dedifferentiation provides an opportunity to probe the molecular underpinnings of cell identity and reprogramming. Zebafish muscle regeneration utilizes dedifferentiation to reprogram mature multinucleated myocytes into dedifferentiated myoblast that re enter the cell cycle. A unique advantage of this system is that the regenerating cell mass is large and fairly homogenous  facilitating genomics approaches to uncovering the underlying biology. Methods: To better understand cellular reprogramming of mature myocytes  we temporally analyzed the changing transcriptome leading up to the proliferative switch. RNA was obtained post Laser Micro dissection LMD of Control  9 xxx post injury HPI or 18 HPI using Trizol and micro column purification. Illumina''s TruSeq Stranded mRNA Library Prep Kit and 0.1   4 µg total mRNA from pooled purified RNA samples were used for performing ribosomal depletion Ribo Zero Gold rRNA Removal Kit  Illumina and library preparation. Sequencing was performed by the UM DNA Sequencing Core  using an Illumina Hi Seq 2000 50 cycle  single end read platform. Results: Clustering and functional annotation of differentially expressed genes highlighted the importance of catabolic and phagocytic processes upregulation at 9 and 18 xxx post injury hpi. Furthermore  genes encoding principle regulators of chromatin states were actively re regulated during the reprogramming process. Utilizing the accessibility of these tissues in the zebrafish model  kKnockdown experiments enabled in vivo validation and phenotypic analysis of candidate genes and pathways for their roles in genomic and cellular reprogramming. Additionally  we found that despite of their low expression levels  lncRNAs were highly represented in gene clusters with dynamic  “switch like” expression profiles  and that miRNA processing was also found important for reprogramming Conclusions:  We conclude that reprogramming of a “post mitotic” myocyte into a dedifferentiated myoblast requires both heritable yet nuanced epigenetic alterations and molecular switches that involve transcription factors  miRNA and lncRNA  while maintaining the lineage restriction of the cell of origin. Overall design: Early time xxx post injury 9 & 18 hours mRNA and lncRNA profiles of Zebrafish lateral eye muscle EOM were generated by deep sequencing  in quadruplicate  using Illumina Hi seq.,,pubmed:29121865,,0 hpi rep1,GSM2430654,,source name:lateral rectus EOM|genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,0 hpi rep1,We checked the quality of the raw reads data for each sample using FastQC version 0.11.3 to identify features of the data that may indicate quality problems e.g. low quality scores  over represented sequences  inappropriate GC content  etc.. We used the software package Tuxedo Suite for alignment  differential expression analysis  and post analysis diagnostics. We aligned reads to the reference genome followed by the transcriptome GRCz10 using TopHat version 2.0.13 and Bowtie version 2.2.1. We used default parameter settings for alignment  with the exception of: “  b2 very sensitive” telling the software to spend extra time searching for valid alignments  and “  max intron length” of 400 kbs. Novel transcript discovery was not performed  employing “  no coverage search” and “  no novel juncs” to limit the read mapping to known transcripts. We used Cufflinks/CuffDiff version 2.2.1 for expression quantitation and differential expression analysis  using NCBI GRCz10.fa as the reference genome sequence and NCBI GRCz10.gtf as the reference transcriptome annotation. For this analysis  we used parameter settings: “  multi read correct” to adjust expression calculations for reads that map in more than one locus  as well as “  compatible hits norm” and “  upper quartile –norm” for normalization of expression values. We generated diagnostic plots using the CummeRbund package. Genome build: GRCz10 Supplementary files format and content: Processed Data Files include annotated fold change tab delimited files and differential expression tab delimited files,lateral rectus EOM,,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,,genotype:actin:GFP|tissue:lateral rectus EOM|xxx post injury:0,GSM2430654,GSM2430654: 0 hpi rep1; Danio rerio; RNA Seq,GSM2430654,,1,Fish heads were were removed  decalcified in ammonium sulfate EDTA mixture  frozen  cryosectioned and lateral rectus isolated by LMD.  RNA was harvested using Trizol reagent followed by Reliaprep tissue Miniprep system. Illumina TruSeq Stranded mRNA Library Prep Kit and 0.1 to 4 ug of total RNA for the construction of sequencing libraries. RNA libraries were prepared for sequencing using standard Illumina protocols,GEO Accession:GSM2430654,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 2000,,SRP095238,,,0hpi_44113.fastq.gz,fastq,2656056728.0,51078014.0,GSM2430654 r1,0:52,A:652742098;C:649243306;G:612049135;T:741907471;N:114718,52,,,,652742098,649243306,612049135,741907471,114718,SRX2431086,SRS1866963,SRA504806,GEO,"Kellogg Eye Center, Ophthalmology and Visual Sciences, University of Michigan",1,0.85198,,0.24059,,0.73357,,0.48804,,52,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,trueseq,bulk,unknown,unknown,,United States,2016-12-16,Undetermined,Adult,Head,Nervous System