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
9812,ERR3931362,ERX3938952,ERS4329529,ERP120057,PRJEB36819,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E-MTAB-8800,Transcriptome Analysis,Kit ligand Kitlg is a pleiotropic cytokine with a prominent role in vertebrate erythropoiesis. Due to whole genome duplication  zebrafish possess two copies of Kit ligand Kitlga and Kitlgb. We generated a recombinant version of Kitlga  tested its biological activity in culture of zebrafish kidney marrow cells and performed RNA seq analysis. Using this assay  we demonstrate that Kitlga cooperates with other factors to promote erythroid cell expansion ex vivo.,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,,Protocols: Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,WKM 7 ED,SAMEA6565186,Institute of Molecular Genetics of the Czech Academy of Sciences,ENA first public:2021 12 31|ENA last update:2021 12 31|External Id:SAMEA6565186|INSDC center alias:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC center name:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC first public:2021 12 31T00:11:11Z|INSDC last update:2021 12 31T00:11:11Z|INSDC status:public|Submitter Id:E MTAB 8800:WKM 7 ED|broker name:ArrayExpress|cell type:erythroid progenitor cell|common name:zebrafish|developmental stage:adult|disease:normal|genotype:Tg gata1:DsRed|growth condition:Erythropoietin  Dexamethas1|individual:WKM7|organism part:head kidney|sample name:E MTAB 8800:WKM 7 ED,,,,,,,,,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E MTAB 8800:WKM 7 ED s,WKM 7 ED s,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,Experimental Factor: stimulus:n1,RNA-Seq,TRANSCRIPTOMIC,Inverse rRNA,SINGLE,ILLUMINA,NextSeq 500,,ERP120057,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,10_WKM_7_ED.fastq.gz,fastq,3603783627.0,47724788.0,E MTAB 8800:WKM 7 ED,0:75.51 1:0,A:730277817;C:1059558661;G:1006087781;T:807771859;N:87509,75,0,,,730277817,1059558661,1006087781,807771859,87509,ERX3938952,ERS4329529,ERA2383450,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,1,0.96114,,0.20335,,0.83798,,0.76524,,76,,B,,usable mapping rate,illumina,nextseq,full_length,rrna_depletion,smarter,bulk,bulk,bulk,,Czech Republic,2021-12-31,Adult,Adult,Multi-tissue,Multi-system
9813,ERR3931361,ERX3938951,ERS4329528,ERP120057,PRJEB36819,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E-MTAB-8800,Transcriptome Analysis,Kit ligand Kitlg is a pleiotropic cytokine with a prominent role in vertebrate erythropoiesis. Due to whole genome duplication  zebrafish possess two copies of Kit ligand Kitlga and Kitlgb. We generated a recombinant version of Kitlga  tested its biological activity in culture of zebrafish kidney marrow cells and performed RNA seq analysis. Using this assay  we demonstrate that Kitlga cooperates with other factors to promote erythroid cell expansion ex vivo.,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,,Protocols: Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,WKM 7 EaD,SAMEA6565185,Institute of Molecular Genetics of the Czech Academy of Sciences,ENA first public:2021 12 31|ENA last update:2021 12 31|External Id:SAMEA6565185|INSDC center alias:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC center name:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC first public:2021 12 31T00:11:11Z|INSDC last update:2021 12 31T00:11:11Z|INSDC status:public|Submitter Id:E MTAB 8800:WKM 7 EaD|broker name:ArrayExpress|cell type:erythroid progenitor cell|common name:zebrafish|developmental stage:adult|disease:normal|genotype:Tg gata1:DsRed|growth condition:Erythropoietin  Dexamethas1|individual:WKM7|organism part:head kidney|sample name:E MTAB 8800:WKM 7 EaD,,,,,,,,,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E MTAB 8800:WKM 7 EaD s,WKM 7 EaD s,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,Experimental Factor: stimulus:kit ligand,RNA-Seq,TRANSCRIPTOMIC,Inverse rRNA,SINGLE,ILLUMINA,NextSeq 500,,ERP120057,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,11_WKM_7_EaD_1.fastq.gz,fastq,3127207407.0,41417754.0,E MTAB 8800:WKM 7 EaD,0:75.50 1:0,A:618290483;C:948661192;G:891134088;T:669046822;N:74822,75,0,,,618290483,948661192,891134088,669046822,74822,ERX3938951,ERS4329528,ERA2383450,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,1,0.96441,,0.20171,,0.85427,,0.75425,,76,,B,,usable mapping rate,illumina,nextseq,full_length,rrna_depletion,smarter,bulk,bulk,bulk,,Czech Republic,2021-12-31,Adult,Adult,Multi-tissue,Multi-system
9814,ERR3931360,ERX3938950,ERS4329527,ERP120057,PRJEB36819,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E-MTAB-8800,Transcriptome Analysis,Kit ligand Kitlg is a pleiotropic cytokine with a prominent role in vertebrate erythropoiesis. Due to whole genome duplication  zebrafish possess two copies of Kit ligand Kitlga and Kitlgb. We generated a recombinant version of Kitlga  tested its biological activity in culture of zebrafish kidney marrow cells and performed RNA seq analysis. Using this assay  we demonstrate that Kitlga cooperates with other factors to promote erythroid cell expansion ex vivo.,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,,Protocols: Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,WKM 5 ED,SAMEA6565184,Institute of Molecular Genetics of the Czech Academy of Sciences,ENA first public:2021 12 31|ENA last update:2021 12 31|External Id:SAMEA6565184|INSDC center alias:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC center name:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC first public:2021 12 31T00:11:11Z|INSDC last update:2021 12 31T00:11:11Z|INSDC status:public|Submitter Id:E MTAB 8800:WKM 5 ED|broker name:ArrayExpress|cell type:erythroid progenitor cell|common name:zebrafish|developmental stage:adult|disease:normal|genotype:Tg gata1:DsRed|growth condition:Erythropoietin  Dexamethas1|individual:WKM5|organism part:head kidney|sample name:E MTAB 8800:WKM 5 ED,,,,,,,,,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E MTAB 8800:WKM 5 ED s,WKM 5 ED s,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,Experimental Factor: stimulus:n1,RNA-Seq,TRANSCRIPTOMIC,Inverse rRNA,SINGLE,ILLUMINA,NextSeq 500,,ERP120057,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,8_WKM_5_ED.fastq.gz,fastq,3762435507.0,49825705.0,E MTAB 8800:WKM 5 ED,0:75.51 1:0,A:760573477;C:1107794761;G:1060998015;T:832975681;N:93573,75,0,,,760573477,1107794761,1060998015,832975681,93573,ERX3938950,ERS4329527,ERA2383450,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,1,0.96233,,0.20628,,0.84141,,0.73601,,75,,B,,usable mapping rate,illumina,nextseq,full_length,rrna_depletion,smarter,bulk,bulk,bulk,,Czech Republic,2021-12-31,Adult,Adult,Multi-tissue,Multi-system
9815,ERR3931359,ERX3938949,ERS4329526,ERP120057,PRJEB36819,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E-MTAB-8800,Transcriptome Analysis,Kit ligand Kitlg is a pleiotropic cytokine with a prominent role in vertebrate erythropoiesis. Due to whole genome duplication  zebrafish possess two copies of Kit ligand Kitlga and Kitlgb. We generated a recombinant version of Kitlga  tested its biological activity in culture of zebrafish kidney marrow cells and performed RNA seq analysis. Using this assay  we demonstrate that Kitlga cooperates with other factors to promote erythroid cell expansion ex vivo.,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,,Protocols: Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,WKM 5 EaD,SAMEA6565183,Institute of Molecular Genetics of the Czech Academy of Sciences,ENA first public:2021 12 31|ENA last update:2021 12 31|External Id:SAMEA6565183|INSDC center alias:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC center name:Institute of Molecular Genetics of the Czech Academy of Sciences|INSDC first public:2021 12 31T00:11:11Z|INSDC last update:2021 12 31T00:11:11Z|INSDC status:public|Submitter Id:E MTAB 8800:WKM 5 EaD|broker name:ArrayExpress|cell type:erythroid progenitor cell|common name:zebrafish|developmental stage:adult|disease:normal|genotype:Tg gata1:DsRed|growth condition:Erythropoietin  Dexamethas1|individual:WKM5|organism part:head kidney|sample name:E MTAB 8800:WKM 5 EaD,,,,,,,,,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,E MTAB 8800:WKM 5 EaD s,WKM 5 EaD s,Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,Zebrafish whole kidney marrow WKM cells were isolated as described in Svoboda  O. et al. Ex vivo tools for the clonal analysis of zebrafish hematopoiesis. Nature protocols 11  1007 1020  doi:10.1038/nprot.2016.053 2016. Total RNA was isolated from 6 7×10 6 WKM cells cultivated in the presence of erythropoietin Epo  dexamethasone Dex or Epo  Dex and Kitlga  according to the PureLink Micro Kit Invitrogen manufacturer's protocol that includes DNase I treatment. The quantity of isolated RNA was measured spectrophotometrically using NanoDrop ND 1000 Thermo Fisher Scientific and its quality was analyzed by Agilent 2100 Bioanalyser Agilent Technologies. RNA integrity number  which is regarded as criteria for high quality total RNA  ranged between 9.5 and 10. Takara SMARTer Stranded Total RNA Seq Kit v2 Takara Bio was used for cDNAlibrary preparation starting with 3.5 ng of total RNA. Library size distribution was evaluated on the Agilent 2100 Bioanalyzer using the High Sensitivity DNA Kit Agilent Technologies.,Experimental Factor: stimulus:kit ligand,RNA-Seq,TRANSCRIPTOMIC,Inverse rRNA,SINGLE,ILLUMINA,NextSeq 500,,ERP120057,NextSeq 500 sequencing; Transcription profiling by RNA seq of zebrafish kidney marrow cells treated with Kitlga,ENA FIRST PUBLIC:2022 01 05|ENA LAST UPDATE:2022 01 05,9_WKM_5_EaD.fastq.gz,fastq,3602342027.0,47707938.0,E MTAB 8800:WKM 5 EaD,0:75.51 1:0,A:717278291;C:1084375347;G:1027250408;T:773351695;N:86286,75,0,,,717278291,1084375347,1027250408,773351695,86286,ERX3938949,ERS4329526,ERA2383450,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,Institute of Molecular Genetics of the Czech Academy of Sciences|European Nucleotide Archive,1,0.96461,,0.20281,,0.85303,,0.74553,,75,,B,,usable mapping rate,illumina,nextseq,full_length,rrna_depletion,smarter,bulk,bulk,bulk,,Czech Republic,2021-12-31,Adult,Adult,Multi-tissue,Multi-system
25196,SRR25685540,SRX21410747,SRS18649229,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 4,GSM7717538,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717538,GSM7717538: Hmga1a overexpression sample 4; Danio rerio; RNA Seq,GSM7717538 r1,GSM7717538,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_OE4_cbc.fastq.gz,fastq,373009260.0,6216821.0,GSM7717538 r1,0:60,A:154344754;C:67291339;G:55785796;T:95519920;N:67451,60,,,,154344754,67291339,55785796,95519920,67451,SRX21410747,SRS18649229,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89552,,0.06993,,0.9276,,0.58138,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25197,SRR25685541,SRX21410747,SRS18649229,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 4,GSM7717538,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717538,GSM7717538: Hmga1a overexpression sample 4; Danio rerio; RNA Seq,GSM7717538 r1,GSM7717538,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_OE4_cbc.fastq.gz,fastq,362301060.0,6038351.0,GSM7717538 r2,0:60,A:106180158;C:75387781;G:73886850;T:106761396;N:84875,60,,,,106180158,75387781,73886850,106761396,84875,SRX21410747,SRS18649229,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89159,,0.06701,,0.87081,,0.62237,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25198,SRR25685542,SRX21410747,SRS18649229,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 4,GSM7717538,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717538,GSM7717538: Hmga1a overexpression sample 4; Danio rerio; RNA Seq,GSM7717538 r1,GSM7717538,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_OE4_cbc.fastq.gz,fastq,384538200.0,6408970.0,GSM7717538 r3,0:60,A:113163070;C:80510291;G:76775008;T:114062728;N:27103,60,,,,113163070,80510291,76775008,114062728,27103,SRX21410747,SRS18649229,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.90032,,0.06985,,0.87008,,0.61631,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25199,SRR25685543,SRX21410747,SRS18649229,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 4,GSM7717538,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717538,GSM7717538: Hmga1a overexpression sample 4; Danio rerio; RNA Seq,GSM7717538 r1,GSM7717538,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_OE4_cbc.fastq.gz,fastq,369674700.0,6161245.0,GSM7717538 r4,0:60,A:108130666;C:76988468;G:75491768;T:109027980;N:35818,60,,,,108130666,76988468,75491768,109027980,35818,SRX21410747,SRS18649229,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89622,,0.06895,,0.86854,,0.61464,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25200,SRR25685544,SRX21410746,SRS18649228,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 3,GSM7717537,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717537,GSM7717537: Hmga1a overexpression sample 3; Danio rerio; RNA Seq,GSM7717537 r1,GSM7717537,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_OE3_cbc.fastq.gz,fastq,172977180.0,2882953.0,GSM7717537 r1,0:60,A:75387211;C:31808233;G:24071421;T:41679068;N:31247,60,,,,75387211,31808233,24071421,41679068,31247,SRX21410746,SRS18649228,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88458,,0.06987,,0.92788,,0.58263,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25201,SRR25685545,SRX21410746,SRS18649228,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 3,GSM7717537,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717537,GSM7717537: Hmga1a overexpression sample 3; Danio rerio; RNA Seq,GSM7717537 r1,GSM7717537,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_OE3_cbc.fastq.gz,fastq,168370020.0,2806167.0,GSM7717537 r2,0:60,A:49447288;C:35622124;G:34182575;T:49078813;N:39220,60,,,,49447288,35622124,34182575,49078813,39220,SRX21410746,SRS18649228,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88366,,0.06639,,0.87519,,0.43134,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25202,SRR25685546,SRX21410746,SRS18649228,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 3,GSM7717537,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717537,GSM7717537: Hmga1a overexpression sample 3; Danio rerio; RNA Seq,GSM7717537 r1,GSM7717537,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_OE3_cbc.fastq.gz,fastq,177341340.0,2955689.0,GSM7717537 r3,0:60,A:52304623;C:37759158;G:35264433;T:52000964;N:12162,60,,,,52304623,37759158,35264433,52000964,12162,SRX21410746,SRS18649228,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.8907,,0.06795,,0.87405,,0.57596,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25203,SRR25685547,SRX21410746,SRS18649228,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 3,GSM7717537,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717537,GSM7717537: Hmga1a overexpression sample 3; Danio rerio; RNA Seq,GSM7717537 r1,GSM7717537,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_OE3_cbc.fastq.gz,fastq,172482600.0,2874710.0,GSM7717537 r4,0:60,A:50610545;C:36521080;G:35043934;T:50291237;N:15804,60,,,,50610545,36521080,35043934,50291237,15804,SRX21410746,SRS18649228,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88558,,0.06686,,0.87373,,0.57425,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25204,SRR25685548,SRX21410745,SRS18649227,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 2,GSM7717536,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717536,GSM7717536: Hmga1a overexpression sample 2; Danio rerio; RNA Seq,GSM7717536 r1,GSM7717536,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_OE2_cbc.fastq.gz,fastq,420273960.0,7004566.0,GSM7717536 r1,0:60,A:172608345;C:77102289;G:65053968;T:105434207;N:75151,60,,,,172608345,77102289,65053968,105434207,75151,SRX21410745,SRS18649227,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.90654,,0.06306,,0.92904,,0.38886,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25205,SRR25685549,SRX21410745,SRS18649227,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 2,GSM7717536,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717536,GSM7717536: Hmga1a overexpression sample 2; Danio rerio; RNA Seq,GSM7717536 r1,GSM7717536,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_OE2_cbc.fastq.gz,fastq,408658800.0,6810980.0,GSM7717536 r2,0:60,A:118741152;C:85204554;G:86928543;T:117687807;N:96744,60,,,,118741152,85204554,86928543,117687807,96744,SRX21410745,SRS18649227,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.90277,,0.06298,,0.87302,,0.66727,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25206,SRR25685550,SRX21410745,SRS18649227,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 2,GSM7717536,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717536,GSM7717536: Hmga1a overexpression sample 2; Danio rerio; RNA Seq,GSM7717536 r1,GSM7717536,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_OE2_cbc.fastq.gz,fastq,433893360.0,7231556.0,GSM7717536 r3,0:60,A:126666020;C:91068379;G:90449908;T:125677088;N:31965,60,,,,126666020,91068379,90449908,125677088,31965,SRX21410745,SRS18649227,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.90833,,0.06364,,0.87351,,0.66644,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25207,SRR25685551,SRX21410745,SRS18649227,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 2,GSM7717536,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717536,GSM7717536: Hmga1a overexpression sample 2; Danio rerio; RNA Seq,GSM7717536 r1,GSM7717536,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_OE2_cbc.fastq.gz,fastq,418311900.0,6971865.0,GSM7717536 r4,0:60,A:121375806;C:87324728;G:89011817;T:120559021;N:40528,60,,,,121375806,87324728,89011817,120559021,40528,SRX21410745,SRS18649227,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.90583,,0.06349,,0.87156,,0.36876,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25208,SRR25685552,SRX21410744,SRS18649226,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 1,GSM7717535,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717535,GSM7717535: Hmga1a overexpression sample 1; Danio rerio; RNA Seq,GSM7717535 r1,GSM7717535,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_OE1_cbc.fastq.gz,fastq,219019680.0,3650328.0,GSM7717535 r1,0:60,A:89205341;C:39777204;G:33514473;T:56486057;N:36605,60,,,,89205341,39777204,33514473,56486057,36605,SRX21410744,SRS18649226,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89316,,0.08503,,0.92125,,0.51486,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25209,SRR25685553,SRX21410744,SRS18649226,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 1,GSM7717535,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717535,GSM7717535: Hmga1a overexpression sample 1; Danio rerio; RNA Seq,GSM7717535 r1,GSM7717535,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_OE1_cbc.fastq.gz,fastq,213035040.0,3550584.0,GSM7717535 r2,0:60,A:60747442;C:44096249;G:44275929;T:63866231;N:49189,60,,,,60747442,44096249,44275929,63866231,49189,SRX21410744,SRS18649226,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89017,,0.08631,,0.86543,,0.52632,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25210,SRR25685554,SRX21410744,SRS18649226,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 1,GSM7717535,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717535,GSM7717535: Hmga1a overexpression sample 1; Danio rerio; RNA Seq,GSM7717535 r1,GSM7717535,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_OE1_cbc.fastq.gz,fastq,226019460.0,3766991.0,GSM7717535 r3,0:60,A:64732665;C:47081812;G:46018051;T:68171208;N:15724,60,,,,64732665,47081812,46018051,68171208,15724,SRX21410744,SRS18649226,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89632,,0.08716,,0.86661,,0.54361,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25211,SRR25685555,SRX21410744,SRS18649226,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,Hmga1a overexpression sample 1,GSM7717535,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,Hmga1a overexpression sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:Hmga1a overexpression|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717535,GSM7717535: Hmga1a overexpression sample 1; Danio rerio; RNA Seq,GSM7717535 r1,GSM7717535,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_OE1_cbc.fastq.gz,fastq,217742460.0,3629041.0,GSM7717535 r4,0:60,A:61973072;C:45113665;G:45294805;T:65339336;N:21582,60,,,,61973072,45113665,45294805,65339336,21582,SRX21410744,SRS18649226,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89237,,0.08517,,0.86454,,0.54639,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25212,SRR25685556,SRX21410743,SRS18649225,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 4,GSM7717534,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717534,GSM7717534: control sample 4; Danio rerio; RNA Seq,GSM7717534 r1,GSM7717534,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_Ctrl4_cbc.fastq.gz,fastq,242809260.0,4046821.0,GSM7717534 r1,0:60,A:101286554;C:44368173;G:36112695;T:60997635;N:44203,60,,,,101286554,44368173,36112695,60997635,44203,SRX21410743,SRS18649225,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.87519,,0.14838,,0.9362,,0.79824,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25213,SRR25685557,SRX21410743,SRS18649225,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 4,GSM7717534,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717534,GSM7717534: control sample 4; Danio rerio; RNA Seq,GSM7717534 r1,GSM7717534,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_Ctrl4_cbc.fastq.gz,fastq,235587720.0,3926462.0,GSM7717534 r2,0:60,A:71954218;C:50127333;G:45371371;T:68077780;N:57018,60,,,,71954218,50127333,45371371,68077780,57018,SRX21410743,SRS18649225,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.8759,,0.14468,,0.88075,,0.74532,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25214,SRR25685558,SRX21410743,SRS18649225,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 4,GSM7717534,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717534,GSM7717534: control sample 4; Danio rerio; RNA Seq,GSM7717534 r1,GSM7717534,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_Ctrl4_cbc.fastq.gz,fastq,248320680.0,4138678.0,GSM7717534 r3,0:60,A:76188968;C:53138643;G:46699955;T:72274599;N:18515,60,,,,76188968,53138643,46699955,72274599,18515,SRX21410743,SRS18649225,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88396,,0.1471,,0.87864,,0.74275,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25215,SRR25685559,SRX21410743,SRS18649225,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 4,GSM7717534,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 4,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717534,GSM7717534: control sample 4; Danio rerio; RNA Seq,GSM7717534 r1,GSM7717534,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_Ctrl4_cbc.fastq.gz,fastq,239678820.0,3994647.0,GSM7717534 r4,0:60,A:73122694;C:51017089;G:46184519;T:69330703;N:23815,60,,,,73122694,51017089,46184519,69330703,23815,SRX21410743,SRS18649225,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88113,,0.14666,,0.88045,,0.79921,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25216,SRR25685560,SRX21410742,SRS18649224,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 3,GSM7717533,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717533,GSM7717533: control sample 3; Danio rerio; RNA Seq,GSM7717533 r1,GSM7717533,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_Ctrl3_cbc.fastq.gz,fastq,164862000.0,2747700.0,GSM7717533 r1,0:60,A:67317722;C:30175032;G:25320195;T:42019155;N:29896,60,,,,67317722,30175032,25320195,42019155,29896,SRX21410742,SRS18649224,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.8874,,0.16231,,0.93513,,0.45903,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25217,SRR25685561,SRX21410742,SRS18649224,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 3,GSM7717533,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717533,GSM7717533: control sample 3; Danio rerio; RNA Seq,GSM7717533 r1,GSM7717533,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_Ctrl3_cbc.fastq.gz,fastq,159878880.0,2664648.0,GSM7717533 r2,0:60,A:48277840;C:33800190;G:31556276;T:46206979;N:37595,60,,,,48277840,33800190,31556276,46206979,37595,SRX21410742,SRS18649224,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.8874,,0.15941,,0.88038,,0.79589,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25218,SRR25685562,SRX21410742,SRS18649224,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 3,GSM7717533,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717533,GSM7717533: control sample 3; Danio rerio; RNA Seq,GSM7717533 r1,GSM7717533,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_Ctrl3_cbc.fastq.gz,fastq,169506240.0,2825104.0,GSM7717533 r3,0:60,A:51435401;C:36027782;G:32684721;T:49346338;N:11998,60,,,,51435401,36027782,32684721,49346338,11998,SRX21410742,SRS18649224,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89554,,0.16117,,0.87947,,0.795,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25219,SRR25685563,SRX21410742,SRS18649224,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 3,GSM7717533,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 3,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717533,GSM7717533: control sample 3; Danio rerio; RNA Seq,GSM7717533 r1,GSM7717533,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_Ctrl3_cbc.fastq.gz,fastq,163347840.0,2722464.0,GSM7717533 r4,0:60,A:49253957;C:34538564;G:32268358;T:47272095;N:14866,60,,,,49253957,34538564,32268358,47272095,14866,SRX21410742,SRS18649224,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89252,,0.15956,,0.8784,,0.79732,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25220,SRR25685564,SRX21410741,SRS18649223,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 2,GSM7717532,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717532,GSM7717532: control sample 2; Danio rerio; RNA Seq,GSM7717532 r1,GSM7717532,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_Ctrl2_cbc.fastq.gz,fastq,19885560.0,331426.0,GSM7717532 r1,0:60,A:8615440;C:3592607;G:2886695;T:4787767;N:3051,60,,,,8615440,3592607,2886695,4787767,3051,SRX21410741,SRS18649223,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.84848,,0.13671,,0.96136,,0.84253,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25221,SRR25685565,SRX21410741,SRS18649223,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 2,GSM7717532,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717532,GSM7717532: control sample 2; Danio rerio; RNA Seq,GSM7717532 r1,GSM7717532,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_Ctrl2_cbc.fastq.gz,fastq,19226760.0,320446.0,GSM7717532 r2,0:60,A:5898378;C:4022375;G:3854218;T:5447181;N:4608,60,,,,5898378,4022375,3854218,5447181,4608,SRX21410741,SRS18649223,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.84542,,0.13731,,0.94004,,0.38758,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25222,SRR25685566,SRX21410741,SRS18649223,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 2,GSM7717532,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717532,GSM7717532: control sample 2; Danio rerio; RNA Seq,GSM7717532 r1,GSM7717532,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_Ctrl2_cbc.fastq.gz,fastq,20360520.0,339342.0,GSM7717532 r3,0:60,A:6273552;C:4289098;G:3982791;T:5813710;N:1369,60,,,,6273552,4289098,3982791,5813710,1369,SRX21410741,SRS18649223,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.85213,,0.13819,,0.93929,,0.83913,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25223,SRR25685567,SRX21410741,SRS18649223,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 2,GSM7717532,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 2,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717532,GSM7717532: control sample 2; Danio rerio; RNA Seq,GSM7717532 r1,GSM7717532,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_Ctrl2_cbc.fastq.gz,fastq,19742340.0,329039.0,GSM7717532 r4,0:60,A:6042722;C:4140425;G:3955209;T:5601961;N:2023,60,,,,6042722,4140425,3955209,5601961,2023,SRX21410741,SRS18649223,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.84722,,0.13682,,0.93933,,0.83301,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25224,SRR25685568,SRX21410740,SRS18649222,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 1,GSM7717531,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717531,GSM7717531: control sample 1; Danio rerio; RNA Seq,GSM7717531 r1,GSM7717531,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L001_Ctrl1_cbc.fastq.gz,fastq,296163420.0,4936057.0,GSM7717531 r1,0:60,A:121966307;C:53233433;G:44972413;T:75936522;N:54745,60,,,,121966307,53233433,44972413,75936522,54745,SRX21410740,SRS18649222,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88546,,0.17055,,0.92681,,0.76028,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25225,SRR25685569,SRX21410740,SRS18649222,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 1,GSM7717531,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717531,GSM7717531: control sample 1; Danio rerio; RNA Seq,GSM7717531 r1,GSM7717531,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L002_Ctrl1_cbc.fastq.gz,fastq,287707980.0,4795133.0,GSM7717531 r2,0:60,A:87738683;C:59468794;G:56448494;T:83984130;N:67879,60,,,,87738683,59468794,56448494,83984130,67879,SRX21410740,SRS18649222,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88284,,0.16626,,0.86561,,0.74308,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25226,SRR25685570,SRX21410740,SRS18649222,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 1,GSM7717531,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717531,GSM7717531: control sample 1; Danio rerio; RNA Seq,GSM7717531 r1,GSM7717531,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L003_Ctrl1_cbc.fastq.gz,fastq,303833460.0,5063891.0,GSM7717531 r3,0:60,A:93092013;C:63221167;G:58235370;T:89262119;N:22791,60,,,,93092013,63221167,58235370,89262119,22791,SRX21410740,SRS18649222,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.89102,,0.16657,,0.86336,,0.75396,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25227,SRR25685571,SRX21410740,SRS18649222,SRP455779,PRJNA1006658,Interspecies comparison reveals Hmga1 as driver of cardiac regeneration [bulk RNAseq Hmga1a OE],GSE241157,Transcriptome Analysis,The prospect of repairing the heart post a myocardial infarction by promoting cardiomyocyte proliferation has gained momentum from studies showing the heart's regenerative ability in fish  amphibians and neonatal mammals. Despite evidence of varying cardiomyocyte proliferation rates among species  the molecular mechanisms driving cardiomyocyte cell cycle re entry remain insufficiently understood. In this study  we employed spatial transcriptomics and identified high mobility group AT hook 1a Hmga1a as being upregulated in cardiomyocytes of the injury border zone in zebrafish  but not in mice. Through knock out and cardiomyocyte specific overexpression of hmga1a  we found that Hmga1a was required for zebrafish heart regeneration and sufficient to drive cardiomyocyte proliferation. In addition  a single injection of Hmga1 virus in injured mouse hearts resulted in increased border zone cardiomyocyte proliferation and improved heart function. Mechanistically  Hmga1 expression reduced repressive H3K27me3 histone modifications from developmentally regulated genes and induced a border zone like transcriptional program in adult cardiomyocytes. Our study demonstrates the value of interspecies comparisons by identifying Hmga1 as a critical driver of heart regeneration and highlights Hmga1 as a promising therapeutic candidate to improve cardiac xxx post injury. Overall design: TOMOseq was performed on mouse and zebrafish hearts at 3  7 and 14 xxx post injury for the interspecies comparison. single cell RNA sequencing was performed on wildtype versus hmga1a mutant zebrafish cardiomyocytes 7 days post cryoinjury to assess differences during heart regeneration. Bulk RNA sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect in an uninjured heart. bulk sortChIC sequencing was performed on control versus Hmga1a overexpression cardiomyocytes to assess the effect of Hmga1a on the chromatin.,parent bioproject:PRJNA1006653,pubmed:39747457,,control sample 1,GSM7717531,,source name:adult heart|tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen|geo loc name:missing|collection date:missing,control sample 1,FASTQ files were mapped with the STARandGO pipeline https://github.com/anna alemany/VASAseq/blob/main/mapping/map star.sh against the danRer11 ENSEMBL genome with the zebrafish Lawson V4.3.2 annotation. Normalization and downstream analysis were performed in R. Due to low read count  samples control 2 and overexpression 1 were excluded from analysis. Using the R package EdgeR  differentially expressed genes were obtained FC < 1 or >1 and Pval<0.05. Gene lists were subjected to GO analysis using the online tool DAVID. Assembly: danrer11 Supplementary files format and content: excel file containing edgeR results and GO analysis results Supplementary files format and content: count table spliced transcriptcounts,adult heart,zebrafish were treated with tamoxifen to induce Hmga1a overexpression,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,tissue:adult heart|genotype 1:cmlc2:dsred|genotype 2:control|cell type:cardiomyocytes|treatment:14 days post tamoxifen,GSM7717531,GSM7717531: control sample 1; Danio rerio; RNA Seq,GSM7717531 r1,GSM7717531,1,Unfixed ventricles were dissociated by Collagenase and TrypLE Express treatment to prepare single cell solutions.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP455779,,,HUB-PN-b004_HHHK2BGXN_S1_L004_Ctrl1_cbc.fastq.gz,fastq,293865840.0,4897764.0,GSM7717531 r4,0:60,A:89531768;C:60796725;G:57688758;T:85819485;N:29104,60,,,,89531768,60796725,57688758,85819485,29104,SRX21410740,SRS18649222,SRA1695358,"Jeroen Bakkers, Hubrecht Institute","Jeroen Bakkers, Hubrecht Institute",1,0.88911,,0.16498,,0.86145,,0.75653,,60,,B,,usable mapping rate,illumina,nextseq,unknown,cdna_unspecified,unknown,sc_generic,bulk,bulk,,Netherlands,2023-08-18,Adult,Adult,Heart,Cardiovascular System
25273,SRR25764091,SRX21486763,SRS18719063,SRP457108,PRJNA1009807,Dynamics of the zebrafish tRNAome during the maternal to zygotic transition [RNA Seq],GSE241752,Transcriptome Analysis,Time course analysis of tRNA abundance during zebrafish early embryonic development. Overall design: Wild type TLAB strain zebrafish embryos were grown in standard housing conditions.Unfertilized eggs 0 hpf were collected or embryos were staged and collected at consecutive developmental time points  namelyat the 256 cell 2.5 hpf  1000 cell 3 hpf  sphere 4 hpf  shield 6 hpf and bud 10 hpf stages. Eggs and embryos were either flash frozen in liquid nitrogen or immediately processed. Samples were used for western blotting analysis  polysome profiling  ribosome profiling or mRNA and tRNA sequencing for investigating the regulation of tRNA gene expression and translational status during early zebrafish embryogenesis.,parent bioproject:PRJNA1009800,pubmed:39402326,,WT bud 10 hpf RNA seq rep2,GSM7734768,,source name:Gastrula|strain:TLAB strain|tissue:Gastrula|developmental stage:Bud 10 hpf|genotype:WT|geo loc name:missing|collection date:missing,WT bud 10 hpf RNA seq rep2,3’ adapters were trimmed using Trim Galore v0.6.4 with default settings  retaining reads of length ≥20. Reads were aligned to the GRCz11 zebrafish genome using STAR v2.6.1c with the following parameters:   outSAMtype BAM SortedByCoordinate   outFilterMultimapNmax 1   outFilterMismatchNmax 1   quantMode TranscriptomeSAM GeneCounts   alignEndsType Local   seedSearchStartLmax 14   alignIntronMax 10000   outFilterIntronMotifs RemoveNoncanonicalUnannotated. featureCounts v1.6.2 was used to count reads overlapping a filtered set of protein coding gene annotations from the GENCODE basic gene annotation. Differential gene expression analysis was performed using DESEq2 v1.38.1 with default settings and gene counts from featureCounts. Assembly: GRCz11 Supplementary files format and content: csv; transcripts per million TPM counts per transcript in MANE annotation,Gastrula,unperturbed growth conditions in E3 medium for zebrafish embryos.,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,Embryos were grown in standard housing conditions namely28°C at a 14/10 hour light/dark cycle.,strain:TLAB strain|tissue:Gastrula|developmental stage:Bud 10 hpf|genotype:WT,GSM7734768,GSM7734768: WT bud 10 hpf RNA seq rep2; Danio rerio; RNA Seq,GSM7734768 r1,GSM7734768,1,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP457108,,,WT_mRNA_bud_2.fastq.gz,fastq,2470912004.0,31168086.0,GSM7734768 r1,0:79.28,A:656817108;C:568241258;G:504262095;T:741507737;N:83806,79,,,,656817108,568241258,504262095,741507737,83806,SRX21486763,SRS18719063,SRA1700431,"Mechanisms of Protein Biogenesis, Max Planck Institute for Biochemistry",Max Planck Institute of Biochemistry,1,0.91479,,0.27298,,0.74231,,0.57302,,79,,B,,usable mapping rate,illumina,nextseq,unknown,small_rna,unknown,bulk,bulk,bulk,,Germany,2023-08-28,Gastrula,Embryo,Whole Organism,All anatomical structures
25274,SRR25764092,SRX21486762,SRS18719064,SRP457108,PRJNA1009807,Dynamics of the zebrafish tRNAome during the maternal to zygotic transition [RNA Seq],GSE241752,Transcriptome Analysis,Time course analysis of tRNA abundance during zebrafish early embryonic development. Overall design: Wild type TLAB strain zebrafish embryos were grown in standard housing conditions.Unfertilized eggs 0 hpf were collected or embryos were staged and collected at consecutive developmental time points  namelyat the 256 cell 2.5 hpf  1000 cell 3 hpf  sphere 4 hpf  shield 6 hpf and bud 10 hpf stages. Eggs and embryos were either flash frozen in liquid nitrogen or immediately processed. Samples were used for western blotting analysis  polysome profiling  ribosome profiling or mRNA and tRNA sequencing for investigating the regulation of tRNA gene expression and translational status during early zebrafish embryogenesis.,parent bioproject:PRJNA1009800,pubmed:39402326,,WT bud 10 hpf RNA seq rep1,GSM7734767,,source name:Gastrula|strain:TLAB strain|tissue:Gastrula|developmental stage:Bud 10 hpf|genotype:WT|geo loc name:missing|collection date:missing,WT bud 10 hpf RNA seq rep1,3’ adapters were trimmed using Trim Galore v0.6.4 with default settings  retaining reads of length ≥20. Reads were aligned to the GRCz11 zebrafish genome using STAR v2.6.1c with the following parameters:   outSAMtype BAM SortedByCoordinate   outFilterMultimapNmax 1   outFilterMismatchNmax 1   quantMode TranscriptomeSAM GeneCounts   alignEndsType Local   seedSearchStartLmax 14   alignIntronMax 10000   outFilterIntronMotifs RemoveNoncanonicalUnannotated. featureCounts v1.6.2 was used to count reads overlapping a filtered set of protein coding gene annotations from the GENCODE basic gene annotation. Differential gene expression analysis was performed using DESEq2 v1.38.1 with default settings and gene counts from featureCounts. Assembly: GRCz11 Supplementary files format and content: csv; transcripts per million TPM counts per transcript in MANE annotation,Gastrula,unperturbed growth conditions in E3 medium for zebrafish embryos.,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,Embryos were grown in standard housing conditions namely28°C at a 14/10 hour light/dark cycle.,strain:TLAB strain|tissue:Gastrula|developmental stage:Bud 10 hpf|genotype:WT,GSM7734767,GSM7734767: WT bud 10 hpf RNA seq rep1; Danio rerio; RNA Seq,GSM7734767 r1,GSM7734767,1,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP457108,,,WT_mRNA_bud_1.fastq.gz,fastq,2153494756.0,27140032.0,GSM7734767 r1,0:79.35,A:560793143;C:508962676;G:445126772;T:638539310;N:72855,79,,,,560793143,508962676,445126772,638539310,72855,SRX21486762,SRS18719064,SRA1700431,"Mechanisms of Protein Biogenesis, Max Planck Institute for Biochemistry",Max Planck Institute of Biochemistry,1,0.88728,,0.25493,,0.74369,,0.56589,,80,,B,,usable mapping rate,illumina,nextseq,unknown,small_rna,unknown,bulk,bulk,bulk,,Germany,2023-08-28,Gastrula,Embryo,Whole Organism,All anatomical structures
25275,SRR25764093,SRX21486761,SRS18719061,SRP457108,PRJNA1009807,Dynamics of the zebrafish tRNAome during the maternal to zygotic transition [RNA Seq],GSE241752,Transcriptome Analysis,Time course analysis of tRNA abundance during zebrafish early embryonic development. Overall design: Wild type TLAB strain zebrafish embryos were grown in standard housing conditions.Unfertilized eggs 0 hpf were collected or embryos were staged and collected at consecutive developmental time points  namelyat the 256 cell 2.5 hpf  1000 cell 3 hpf  sphere 4 hpf  shield 6 hpf and bud 10 hpf stages. Eggs and embryos were either flash frozen in liquid nitrogen or immediately processed. Samples were used for western blotting analysis  polysome profiling  ribosome profiling or mRNA and tRNA sequencing for investigating the regulation of tRNA gene expression and translational status during early zebrafish embryogenesis.,parent bioproject:PRJNA1009800,pubmed:39402326,,WT sphere 4 hpf RNA seq rep2,GSM7734766,,source name:Blastula|strain:TLAB strain|tissue:Blastula|developmental stage:Sphere 4 hpf|genotype:WT|geo loc name:missing|collection date:missing,WT sphere 4 hpf RNA seq rep2,3’ adapters were trimmed using Trim Galore v0.6.4 with default settings  retaining reads of length ≥20. Reads were aligned to the GRCz11 zebrafish genome using STAR v2.6.1c with the following parameters:   outSAMtype BAM SortedByCoordinate   outFilterMultimapNmax 1   outFilterMismatchNmax 1   quantMode TranscriptomeSAM GeneCounts   alignEndsType Local   seedSearchStartLmax 14   alignIntronMax 10000   outFilterIntronMotifs RemoveNoncanonicalUnannotated. featureCounts v1.6.2 was used to count reads overlapping a filtered set of protein coding gene annotations from the GENCODE basic gene annotation. Differential gene expression analysis was performed using DESEq2 v1.38.1 with default settings and gene counts from featureCounts. Assembly: GRCz11 Supplementary files format and content: csv; transcripts per million TPM counts per transcript in MANE annotation,Blastula,unperturbed growth conditions in E3 medium for zebrafish embryos.,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,Embryos were grown in standard housing conditions namely28°C at a 14/10 hour light/dark cycle.,strain:TLAB strain|tissue:Blastula|developmental stage:Sphere 4 hpf|genotype:WT,GSM7734766,GSM7734766: WT sphere 4 hpf RNA seq rep2; Danio rerio; RNA Seq,GSM7734766 r1,GSM7734766,1,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP457108,,,WT_mRNA_sphere_2.fastq.gz,fastq,2455317157.0,30934591.0,GSM7734766 r1,0:79.37,A:614860604;C:588586084;G:522132289;T:729655621;N:82559,79,,,,614860604,588586084,522132289,729655621,82559,SRX21486761,SRS18719061,SRA1700431,"Mechanisms of Protein Biogenesis, Max Planck Institute for Biochemistry",Max Planck Institute of Biochemistry,1,0.94124,,0.10502,,0.74876,,0.57752,,80,,B,,usable mapping rate,illumina,nextseq,unknown,small_rna,unknown,bulk,bulk,bulk,,Germany,2023-08-28,Blastula,Embryo,Whole Organism,All anatomical structures
25276,SRR25764094,SRX21486760,SRS18719060,SRP457108,PRJNA1009807,Dynamics of the zebrafish tRNAome during the maternal to zygotic transition [RNA Seq],GSE241752,Transcriptome Analysis,Time course analysis of tRNA abundance during zebrafish early embryonic development. Overall design: Wild type TLAB strain zebrafish embryos were grown in standard housing conditions.Unfertilized eggs 0 hpf were collected or embryos were staged and collected at consecutive developmental time points  namelyat the 256 cell 2.5 hpf  1000 cell 3 hpf  sphere 4 hpf  shield 6 hpf and bud 10 hpf stages. Eggs and embryos were either flash frozen in liquid nitrogen or immediately processed. Samples were used for western blotting analysis  polysome profiling  ribosome profiling or mRNA and tRNA sequencing for investigating the regulation of tRNA gene expression and translational status during early zebrafish embryogenesis.,parent bioproject:PRJNA1009800,pubmed:39402326,,WT sphere 4 hpf RNA seq rep1,GSM7734765,,source name:Blastula|strain:TLAB strain|tissue:Blastula|developmental stage:Sphere 4 hpf|genotype:WT|geo loc name:missing|collection date:missing,WT sphere 4 hpf RNA seq rep1,3’ adapters were trimmed using Trim Galore v0.6.4 with default settings  retaining reads of length ≥20. Reads were aligned to the GRCz11 zebrafish genome using STAR v2.6.1c with the following parameters:   outSAMtype BAM SortedByCoordinate   outFilterMultimapNmax 1   outFilterMismatchNmax 1   quantMode TranscriptomeSAM GeneCounts   alignEndsType Local   seedSearchStartLmax 14   alignIntronMax 10000   outFilterIntronMotifs RemoveNoncanonicalUnannotated. featureCounts v1.6.2 was used to count reads overlapping a filtered set of protein coding gene annotations from the GENCODE basic gene annotation. Differential gene expression analysis was performed using DESEq2 v1.38.1 with default settings and gene counts from featureCounts. Assembly: GRCz11 Supplementary files format and content: csv; transcripts per million TPM counts per transcript in MANE annotation,Blastula,unperturbed growth conditions in E3 medium for zebrafish embryos.,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,Embryos were grown in standard housing conditions namely28°C at a 14/10 hour light/dark cycle.,strain:TLAB strain|tissue:Blastula|developmental stage:Sphere 4 hpf|genotype:WT,GSM7734765,GSM7734765: WT sphere 4 hpf RNA seq rep1; Danio rerio; RNA Seq,GSM7734765 r1,GSM7734765,1,50 whole embryos were collected per sample and immediately lysed in 800uL LiDS/LET buffer5% Lithium dodecyl sulfate in 20 mM Tris HCl pH=7.4  100 mM LiCl  2 mM EDTA  5 mM DTT  pH 7.4. 250 ng of the same total RNA used for mim tRNAseq library preparation were used for mRNA Seq library construction with the Zymo Seq RiboFree Total RNA Library Kit Zymo Research  #R3000. Libraries were sequenced on a NextSeq 500 platform.,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,NextSeq 500,,SRP457108,,,WT_mRNA_sphere_1.fastq.gz,fastq,2399640874.0,30232118.0,GSM7734765 r1,0:79.37,A:589069860;C:593745131;G:511439690;T:705305674;N:80519,79,,,,589069860,593745131,511439690,705305674,80519,SRX21486760,SRS18719060,SRA1700431,"Mechanisms of Protein Biogenesis, Max Planck Institute for Biochemistry",Max Planck Institute of Biochemistry,1,0.85882,,0.11848,,0.75122,,0.5883,,80,,B,,usable mapping rate,illumina,nextseq,unknown,small_rna,unknown,bulk,bulk,bulk,,Germany,2023-08-28,Blastula,Embryo,Whole Organism,All anatomical structures
28113,SRR26209648,SRX21920662,SRS19005181,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 3,GSM7812991,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812991,GSM7812991: unDMSO t1 WT 3; Danio rerio; RNA Seq,GSM7812991 r1,GSM7812991,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A30_S48_L005_R1_001.fastq.gz,fastq,616449359.0,6103459.0,GSM7812991 r1,0:101,A:152808626;C:149738763;G:141639387;T:172257280;N:5303,101,,,,152808626,149738763,141639387,172257280,5303,SRX21920662,SRS19005181,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94246,,0.08766,,0.69443,,0.4842,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28114,SRR26209649,SRX21920662,SRS19005181,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 3,GSM7812991,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812991,GSM7812991: unDMSO t1 WT 3; Danio rerio; RNA Seq,GSM7812991 r1,GSM7812991,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A30_S48_L006_R1_001.fastq.gz,fastq,609999297.0,6039597.0,GSM7812991 r2,0:101,A:151226657;C:148143193;G:140088806;T:170530812;N:9829,101,,,,151226657,148143193,140088806,170530812,9829,SRX21920662,SRS19005181,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94201,,0.08569,,0.69572,,0.48692,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28115,SRR26209650,SRX21920662,SRS19005181,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 3,GSM7812991,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812991,GSM7812991: unDMSO t1 WT 3; Danio rerio; RNA Seq,GSM7812991 r1,GSM7812991,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A30_S48_L007_R1_001.fastq.gz,fastq,543730470.0,5383470.0,GSM7812991 r3,0:101,A:134685766;C:132190291;G:124881864;T:151967639;N:4910,101,,,,134685766,132190291,124881864,151967639,4910,SRX21920662,SRS19005181,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.9431,,0.08733,,0.69524,,0.48528,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28116,SRR26209651,SRX21920662,SRS19005181,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 3,GSM7812991,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812991,GSM7812991: unDMSO t1 WT 3; Danio rerio; RNA Seq,GSM7812991 r1,GSM7812991,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A30_S16_L007_R1_001.fastq.gz,fastq,649354149.0,6429249.0,GSM7812991 r4,0:101,A:160756303;C:158145998;G:149623680;T:180816390;N:11778,101,,,,160756303,158145998,149623680,180816390,11778,SRX21920662,SRS19005181,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94438,,0.08618,,0.69473,,0.48809,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28117,SRR26209752,SRX21920662,SRS19005181,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 3,GSM7812991,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812991,GSM7812991: unDMSO t1 WT 3; Danio rerio; RNA Seq,GSM7812991 r1,GSM7812991,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A30_S16_L008_R1_001.fastq.gz,fastq,650450504.0,6440104.0,GSM7812991 r5,0:101,A:161054597;C:158340761;G:149784923;T:181251361;N:18862,101,,,,161054597,158340761,149784923,181251361,18862,SRX21920662,SRS19005181,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94338,,0.08713,,0.6968,,0.48443,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28118,SRR26209652,SRX21920661,SRS19005180,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 2,GSM7812990,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812990,GSM7812990: unDMSO t1 WT 2; Danio rerio; RNA Seq,GSM7812990 r1,GSM7812990,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A29_S46_L005_R1_001.fastq.gz,fastq,593068162.0,5871962.0,GSM7812990 r1,0:101,A:147906639;C:143944406;G:137307101;T:163904929;N:5087,101,,,,147906639,143944406,137307101,163904929,5087,SRX21920661,SRS19005180,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94371,,0.06473,,0.69378,,0.47765,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28119,SRR26209653,SRX21920661,SRS19005180,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 2,GSM7812990,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812990,GSM7812990: unDMSO t1 WT 2; Danio rerio; RNA Seq,GSM7812990 r1,GSM7812990,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A29_S46_L006_R1_001.fastq.gz,fastq,588323081.0,5824981.0,GSM7812990 r2,0:101,A:146630863;C:142829925;G:136124185;T:162728186;N:9922,101,,,,146630863,142829925,136124185,162728186,9922,SRX21920661,SRS19005180,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94282,,0.06357,,0.69418,,0.47665,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28120,SRR26209654,SRX21920661,SRS19005180,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 2,GSM7812990,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812990,GSM7812990: unDMSO t1 WT 2; Danio rerio; RNA Seq,GSM7812990 r1,GSM7812990,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A29_S46_L007_R1_001.fastq.gz,fastq,521265747.0,5161047.0,GSM7812990 r3,0:101,A:129905878;C:126622019;G:120526207;T:144206853;N:4790,101,,,,129905878,126622019,120526207,144206853,4790,SRX21920661,SRS19005180,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94508,,0.06499,,0.69367,,0.4834,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28121,SRR26209655,SRX21920661,SRS19005180,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 2,GSM7812990,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812990,GSM7812990: unDMSO t1 WT 2; Danio rerio; RNA Seq,GSM7812990 r1,GSM7812990,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A29_S26_L007_R1_001.fastq.gz,fastq,623834580.0,6176580.0,GSM7812990 r4,0:101,A:155642981;C:151651242;G:144681951;T:171847192;N:11214,101,,,,155642981,151651242,144681951,171847192,11214,SRX21920661,SRS19005180,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94531,,0.06514,,0.69225,,0.48187,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28122,SRR26209656,SRX21920661,SRS19005180,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 2,GSM7812990,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812990,GSM7812990: unDMSO t1 WT 2; Danio rerio; RNA Seq,GSM7812990 r1,GSM7812990,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A29_S26_L008_R1_001.fastq.gz,fastq,622155960.0,6159960.0,GSM7812990 r5,0:101,A:155145221;C:151231599;G:144290581;T:171470641;N:17918,101,,,,155145221,151231599,144290581,171470641,17918,SRX21920661,SRS19005180,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94319,,0.06413,,0.69449,,0.48159,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28123,SRR26209657,SRX21920660,SRS19005179,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 1,GSM7812989,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812989,GSM7812989: unDMSO t1 WT 1; Danio rerio; RNA Seq,GSM7812989 r1,GSM7812989,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A28_S45_L005_R1_001.fastq.gz,fastq,602520550.0,5965550.0,GSM7812989 r1,0:101,A:149619230;C:146559346;G:139674646;T:166662143;N:5185,101,,,,149619230,146559346,139674646,166662143,5185,SRX21920660,SRS19005179,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94449,,0.06296,,0.69487,,0.48,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28124,SRR26209658,SRX21920660,SRS19005179,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 1,GSM7812989,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812989,GSM7812989: unDMSO t1 WT 1; Danio rerio; RNA Seq,GSM7812989 r1,GSM7812989,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A28_S45_L006_R1_001.fastq.gz,fastq,596942522.0,5910322.0,GSM7812989 r2,0:101,A:148193962;C:145221539;G:138267073;T:165249833;N:10115,101,,,,148193962,145221539,138267073,165249833,10115,SRX21920660,SRS19005179,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.9446,,0.06327,,0.69562,,0.48183,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28125,SRR26209659,SRX21920660,SRS19005179,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 1,GSM7812989,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812989,GSM7812989: unDMSO t1 WT 1; Danio rerio; RNA Seq,GSM7812989 r1,GSM7812989,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A28_S45_L007_R1_001.fastq.gz,fastq,532539064.0,5272664.0,GSM7812989 r3,0:101,A:132217323;C:129660296;G:123303893;T:147352732;N:4820,101,,,,132217323,129660296,123303893,147352732,4820,SRX21920660,SRS19005179,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94579,,0.06237,,0.69554,,0.46658,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28126,SRR26209660,SRX21920660,SRS19005179,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 1,GSM7812989,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812989,GSM7812989: unDMSO t1 WT 1; Danio rerio; RNA Seq,GSM7812989 r1,GSM7812989,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A28_S29_L007_R1_001.fastq.gz,fastq,633337569.0,6270669.0,GSM7812989 r4,0:101,A:157286526;C:154336036;G:147137950;T:174565295;N:11762,101,,,,157286526,154336036,147137950,174565295,11762,SRX21920660,SRS19005179,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94562,,0.06294,,0.69489,,0.47406,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28127,SRR26209661,SRX21920660,SRS19005179,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 WT 1,GSM7812989,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 WT 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:unDMSO,GSM7812989,GSM7812989: unDMSO t1 WT 1; Danio rerio; RNA Seq,GSM7812989 r1,GSM7812989,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A28_S29_L008_R1_001.fastq.gz,fastq,636051540.0,6297540.0,GSM7812989 r5,0:101,A:157845668;C:154972063;G:147765532;T:175449801;N:18476,101,,,,157845668,154972063,147765532,175449801,18476,SRX21920660,SRS19005179,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.9471,,0.06288,,0.69536,,0.4797,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28128,SRR26209662,SRX21920659,SRS19005178,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 3,GSM7812988,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812988,GSM7812988: unDMSO t1 K2 3; Danio rerio; RNA Seq,GSM7812988 r1,GSM7812988,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A36_S54_L005_R1_001.fastq.gz,fastq,674188635.0,6675135.0,GSM7812988 r1,0:101,A:173104307;C:161481671;G:152542615;T:187053812;N:6230,101,,,,173104307,161481671,152542615,187053812,6230,SRX21920659,SRS19005178,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94039,,0.07795,,0.69877,,0.48386,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28129,SRR26209663,SRX21920659,SRS19005178,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 3,GSM7812988,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812988,GSM7812988: unDMSO t1 K2 3; Danio rerio; RNA Seq,GSM7812988 r1,GSM7812988,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A36_S54_L006_R1_001.fastq.gz,fastq,667048339.0,6604439.0,GSM7812988 r2,0:101,A:171316049;C:159786547;G:150743446;T:185190228;N:12069,101,,,,171316049,159786547,150743446,185190228,12069,SRX21920659,SRS19005178,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94064,,0.07881,,0.69767,,0.48162,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28130,SRR26209664,SRX21920659,SRS19005178,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 3,GSM7812988,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812988,GSM7812988: unDMSO t1 K2 3; Danio rerio; RNA Seq,GSM7812988 r1,GSM7812988,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A36_S54_L007_R1_001.fastq.gz,fastq,596645683.0,5907383.0,GSM7812988 r3,0:101,A:153131508;C:143126741;G:134745614;T:165635953;N:5867,101,,,,153131508,143126741,134745614,165635953,5867,SRX21920659,SRS19005178,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94156,,0.07795,,0.69751,,0.4833,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28131,SRR26209665,SRX21920659,SRS19005178,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 3,GSM7812988,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812988,GSM7812988: unDMSO t1 K2 3; Danio rerio; RNA Seq,GSM7812988 r1,GSM7812988,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A36_S12_L007_R1_001.fastq.gz,fastq,712385926.0,7053326.0,GSM7812988 r4,0:101,A:183100436;C:171026605;G:161510527;T:196734608;N:13750,101,,,,183100436,171026605,161510527,196734608,13750,SRX21920659,SRS19005178,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94298,,0.07892,,0.6997,,0.48331,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28132,SRR26209666,SRX21920659,SRS19005178,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 3,GSM7812988,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812988,GSM7812988: unDMSO t1 K2 3; Danio rerio; RNA Seq,GSM7812988 r1,GSM7812988,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A36_S12_L008_R1_001.fastq.gz,fastq,714661355.0,7075855.0,GSM7812988 r5,0:101,A:183454698;C:171554090;G:162064705;T:197567065;N:20797,101,,,,183454698,171554090,162064705,197567065,20797,SRX21920659,SRS19005178,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94316,,0.07877,,0.70051,,0.48354,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28133,SRR26209667,SRX21920658,SRS19005177,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 2,GSM7812987,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812987,GSM7812987: unDMSO t1 K2 2; Danio rerio; RNA Seq,GSM7812987 r1,GSM7812987,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A35_S53_L005_R1_001.fastq.gz,fastq,611900723.0,6058423.0,GSM7812987 r1,0:101,A:154668392;C:147817141;G:139653400;T:169756342;N:5448,101,,,,154668392,147817141,139653400,169756342,5448,SRX21920658,SRS19005177,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94636,,0.08022,,0.69962,,0.48201,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28134,SRR26209668,SRX21920658,SRS19005177,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 2,GSM7812987,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812987,GSM7812987: unDMSO t1 K2 2; Danio rerio; RNA Seq,GSM7812987 r1,GSM7812987,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A35_S53_L006_R1_001.fastq.gz,fastq,602971818.0,5970018.0,GSM7812987 r2,0:101,A:152346877;C:145640105;G:137576284;T:167398281;N:10271,101,,,,152346877,145640105,137576284,167398281,10271,SRX21920658,SRS19005177,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94549,,0.08086,,0.69781,,0.47842,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28135,SRR26209669,SRX21920658,SRS19005177,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 2,GSM7812987,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812987,GSM7812987: unDMSO t1 K2 2; Danio rerio; RNA Seq,GSM7812987 r1,GSM7812987,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A35_S53_L007_R1_001.fastq.gz,fastq,539246575.0,5339075.0,GSM7812987 r3,0:101,A:136317506;C:130390122;G:122927887;T:149606028;N:5032,101,,,,136317506,130390122,122927887,149606028,5032,SRX21920658,SRS19005177,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94653,,0.08075,,0.69704,,0.48374,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28136,SRR26209670,SRX21920658,SRS19005177,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 2,GSM7812987,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812987,GSM7812987: unDMSO t1 K2 2; Danio rerio; RNA Seq,GSM7812987 r1,GSM7812987,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A35_S47_L007_R1_001.fastq.gz,fastq,643197593.0,6368293.0,GSM7812987 r4,0:101,A:162743675;C:155711536;G:147135700;T:177594459;N:12223,101,,,,162743675,155711536,147135700,177594459,12223,SRX21920658,SRS19005177,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94757,,0.08023,,0.70055,,0.48458,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28137,SRR26209671,SRX21920658,SRS19005177,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 2,GSM7812987,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812987,GSM7812987: unDMSO t1 K2 2; Danio rerio; RNA Seq,GSM7812987 r1,GSM7812987,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A35_S47_L008_R1_001.fastq.gz,fastq,644356063.0,6379763.0,GSM7812987 r5,0:101,A:162915651;C:155935181;G:147406641;T:178079118;N:19472,101,,,,162915651,155935181,147406641,178079118,19472,SRX21920658,SRS19005177,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94817,,0.08218,,0.70017,,0.48286,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28138,SRR26209672,SRX21920657,SRS19005176,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 1,GSM7812986,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812986,GSM7812986: unDMSO t1 K2 1; Danio rerio; RNA Seq,GSM7812986 r1,GSM7812986,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A34_S52_L005_R1_001.fastq.gz,fastq,615996374.0,6098974.0,GSM7812986 r1,0:101,A:156934542;C:147417998;G:139301915;T:172336421;N:5498,101,,,,156934542,147417998,139301915,172336421,5498,SRX21920657,SRS19005176,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94179,,0.07628,,0.69512,,0.48041,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28139,SRR26209673,SRX21920657,SRS19005176,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 1,GSM7812986,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812986,GSM7812986: unDMSO t1 K2 1; Danio rerio; RNA Seq,GSM7812986 r1,GSM7812986,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A34_S52_L006_R1_001.fastq.gz,fastq,608875571.0,6028471.0,GSM7812986 r2,0:101,A:155127967;C:145701864;G:137575885;T:170459017;N:10838,101,,,,155127967,145701864,137575885,170459017,10838,SRX21920657,SRS19005176,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94248,,0.07563,,0.69512,,0.47982,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28140,SRR26209674,SRX21920657,SRS19005176,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 1,GSM7812986,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812986,GSM7812986: unDMSO t1 K2 1; Danio rerio; RNA Seq,GSM7812986 r1,GSM7812986,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A34_S52_L007_R1_001.fastq.gz,fastq,539739455.0,5343955.0,GSM7812986 r3,0:101,A:137431217;C:129328124;G:121891472;T:151083373;N:5269,101,,,,137431217,129328124,121891472,151083373,5269,SRX21920657,SRS19005176,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.9438,,0.07511,,0.69654,,0.48083,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28141,SRR26209675,SRX21920657,SRS19005176,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 1,GSM7812986,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812986,GSM7812986: unDMSO t1 K2 1; Danio rerio; RNA Seq,GSM7812986 r1,GSM7812986,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A34_S65_L007_R1_001.fastq.gz,fastq,648984489.0,6425589.0,GSM7812986 r4,0:101,A:165552674;C:155580501;G:147078092;T:180761105;N:12117,101,,,,165552674,155580501,147078092,180761105,12117,SRX21920657,SRS19005176,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94513,,0.07694,,0.69451,,0.48174,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28142,SRR26209676,SRX21920657,SRS19005176,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K2 1,GSM7812986,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K2 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K2|treatment:unDMSO,GSM7812986,GSM7812986: unDMSO t1 K2 1; Danio rerio; RNA Seq,GSM7812986 r1,GSM7812986,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A34_S65_L008_R1_001.fastq.gz,fastq,651988330.0,6455330.0,GSM7812986 r5,0:101,A:166130853;C:156282200;G:147738788;T:181817695;N:18794,101,,,,166130853,156282200,147738788,181817695,18794,SRX21920657,SRS19005176,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94437,,0.0759,,0.69597,,0.48083,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28143,SRR26209677,SRX21920656,SRS19005175,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 3,GSM7812985,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812985,GSM7812985: unDMSO t1 K1 3; Danio rerio; RNA Seq,GSM7812985 r1,GSM7812985,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A33_S51_L005_R1_001.fastq.gz,fastq,621669544.0,6155144.0,GSM7812985 r1,0:101,A:157346917;C:148083763;G:141122336;T:175110946;N:5582,101,,,,157346917,148083763,141122336,175110946,5582,SRX21920656,SRS19005175,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94207,,0.06859,,0.69473,,0.48838,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28144,SRR26209678,SRX21920656,SRS19005175,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 3,GSM7812985,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812985,GSM7812985: unDMSO t1 K1 3; Danio rerio; RNA Seq,GSM7812985 r1,GSM7812985,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A33_S51_L006_R1_001.fastq.gz,fastq,613437842.0,6073642.0,GSM7812985 r2,0:101,A:155200714;C:146135271;G:139223090;T:172868018;N:10749,101,,,,155200714,146135271,139223090,172868018,10749,SRX21920656,SRS19005175,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94144,,0.06885,,0.69471,,0.48996,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28145,SRR26209679,SRX21920656,SRS19005175,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 3,GSM7812985,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812985,GSM7812985: unDMSO t1 K1 3; Danio rerio; RNA Seq,GSM7812985 r1,GSM7812985,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A33_S51_L007_R1_001.fastq.gz,fastq,546684518.0,5412718.0,GSM7812985 r3,0:101,A:138292090;C:130364936;G:123978492;T:154043685;N:5315,101,,,,138292090,130364936,123978492,154043685,5315,SRX21920656,SRS19005175,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94375,,0.06988,,0.69589,,0.48741,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28146,SRR26209680,SRX21920656,SRS19005175,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 3,GSM7812985,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812985,GSM7812985: unDMSO t1 K1 3; Danio rerio; RNA Seq,GSM7812985 r1,GSM7812985,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A33_S43_L007_R1_001.fastq.gz,fastq,651065089.0,6446189.0,GSM7812985 r4,0:101,A:164874330;C:155389435;G:148130531;T:182658473;N:12320,101,,,,164874330,155389435,148130531,182658473,12320,SRX21920656,SRS19005175,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94247,,0.06954,,0.69538,,0.48283,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28147,SRR26209681,SRX21920656,SRS19005175,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 3,GSM7812985,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812985,GSM7812985: unDMSO t1 K1 3; Danio rerio; RNA Seq,GSM7812985 r1,GSM7812985,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A33_S43_L008_R1_001.fastq.gz,fastq,652838952.0,6463752.0,GSM7812985 r5,0:101,A:165235507;C:155756581;G:148483290;T:183344035;N:19539,101,,,,165235507,155756581,148483290,183344035,19539,SRX21920656,SRS19005175,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94297,,0.06917,,0.69593,,0.4827,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28148,SRR26209682,SRX21920655,SRS19005174,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 2,GSM7812984,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812984,GSM7812984: unDMSO t1 K1 2; Danio rerio; RNA Seq,GSM7812984 r1,GSM7812984,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A32_S50_L005_R1_001.fastq.gz,fastq,531938215.0,5266715.0,GSM7812984 r1,0:101,A:131083905;C:128715617;G:122601298;T:149532970;N:4425,101,,,,131083905,128715617,122601298,149532970,4425,SRX21920655,SRS19005174,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94249,,0.07108,,0.69485,,0.47386,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28149,SRR26209683,SRX21920655,SRS19005174,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 2,GSM7812984,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812984,GSM7812984: unDMSO t1 K1 2; Danio rerio; RNA Seq,GSM7812984 r1,GSM7812984,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A32_S50_L006_R1_001.fastq.gz,fastq,527781863.0,5225563.0,GSM7812984 r2,0:101,A:130119726;C:127646784;G:121549831;T:148456993;N:8529,101,,,,130119726,127646784,121549831,148456993,8529,SRX21920655,SRS19005174,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94199,,0.0713,,0.69337,,0.473,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28150,SRR26209684,SRX21920655,SRS19005174,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 2,GSM7812984,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812984,GSM7812984: unDMSO t1 K1 2; Danio rerio; RNA Seq,GSM7812984 r1,GSM7812984,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A32_S50_L007_R1_001.fastq.gz,fastq,472785040.0,4681040.0,GSM7812984 r3,0:101,A:116503463;C:114489771;G:108989839;T:132797698;N:4269,101,,,,116503463,114489771,108989839,132797698,4269,SRX21920655,SRS19005174,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94373,,0.07285,,0.69467,,0.47913,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28151,SRR26209685,SRX21920655,SRS19005174,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 2,GSM7812984,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812984,GSM7812984: unDMSO t1 K1 2; Danio rerio; RNA Seq,GSM7812984 r1,GSM7812984,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A32_S71_L007_R1_001.fastq.gz,fastq,561056414.0,5555014.0,GSM7812984 r4,0:101,A:138240115;C:136040813;G:129592563;T:157172399;N:10524,101,,,,138240115,136040813,129592563,157172399,10524,SRX21920655,SRS19005174,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94357,,0.07109,,0.69544,,0.47169,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28152,SRR26209686,SRX21920655,SRS19005174,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 2,GSM7812984,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812984,GSM7812984: unDMSO t1 K1 2; Danio rerio; RNA Seq,GSM7812984 r1,GSM7812984,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A32_S71_L008_R1_001.fastq.gz,fastq,563109744.0,5575344.0,GSM7812984 r5,0:101,A:138778764;C:136444809;G:129964766;T:157904708;N:16697,101,,,,138778764,136444809,129964766,157904708,16697,SRX21920655,SRS19005174,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94358,,0.07253,,0.69345,,0.47443,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28153,SRR26209687,SRX21920654,SRS19005173,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 1,GSM7812983,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812983,GSM7812983: unDMSO t1 K1 1; Danio rerio; RNA Seq,GSM7812983 r1,GSM7812983,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A31_S49_L005_R1_001.fastq.gz,fastq,576725857.0,5710157.0,GSM7812983 r1,0:101,A:142557020;C:140092748;G:133378036;T:160693137;N:4916,101,,,,142557020,140092748,133378036,160693137,4916,SRX21920654,SRS19005173,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94239,,0.07259,,0.69398,,0.47675,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28154,SRR26209688,SRX21920654,SRS19005173,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 1,GSM7812983,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812983,GSM7812983: unDMSO t1 K1 1; Danio rerio; RNA Seq,GSM7812983 r1,GSM7812983,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A31_S49_L006_R1_001.fastq.gz,fastq,569166310.0,5635310.0,GSM7812983 r2,0:101,A:140702145;C:138232540;G:131558917;T:158663414;N:9294,101,,,,140702145,138232540,131558917,158663414,9294,SRX21920654,SRS19005173,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94221,,0.07252,,0.69524,,0.4833,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28155,SRR26209689,SRX21920654,SRS19005173,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 1,GSM7812983,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812983,GSM7812983: unDMSO t1 K1 1; Danio rerio; RNA Seq,GSM7812983 r1,GSM7812983,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A31_S49_L007_R1_001.fastq.gz,fastq,505699425.0,5006925.0,GSM7812983 r3,0:101,A:124940125;C:122891114;G:116919354;T:140944307;N:4525,101,,,,124940125,122891114,116919354,140944307,4525,SRX21920654,SRS19005173,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.944,,0.07242,,0.69473,,0.48289,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28156,SRR26209690,SRX21920654,SRS19005173,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 1,GSM7812983,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812983,GSM7812983: unDMSO t1 K1 1; Danio rerio; RNA Seq,GSM7812983 r1,GSM7812983,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A31_S27_L007_R1_001.fastq.gz,fastq,598624374.0,5926974.0,GSM7812983 r4,0:101,A:147863525;C:145723385;G:138724140;T:166302217;N:11107,101,,,,147863525,145723385,138724140,166302217,11107,SRX21920654,SRS19005173,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94426,,0.07312,,0.69479,,0.48056,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28157,SRR26209691,SRX21920654,SRS19005173,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,unDMSO t1 K1 1,GSM7812983,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO|geo loc name:missing|collection date:missing,unDMSO t1 K1 1,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:K1|treatment:unDMSO,GSM7812983,GSM7812983: unDMSO t1 K1 1; Danio rerio; RNA Seq,GSM7812983 r1,GSM7812983,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A31_S27_L008_R1_001.fastq.gz,fastq,602654072.0,5966872.0,GSM7812983 r5,0:101,A:148869054;C:146693906;G:139571739;T:167501958;N:17415,101,,,,148869054,146693906,139571739,167501958,17415,SRX21920654,SRS19005173,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.9433,,0.0732,,0.69552,,0.47807,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28158,SRR26209692,SRX21920653,SRS19005172,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 3,GSM7812982,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812982,GSM7812982: IR t2 WT 3; Danio rerio; RNA Seq,GSM7812982 r1,GSM7812982,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A21_S38_L005_R1_001.fastq.gz,fastq,617990619.0,6118719.0,GSM7812982 r1,0:101,A:155764078;C:148642484;G:140551460;T:173027146;N:5451,101,,,,155764078,148642484,140551460,173027146,5451,SRX21920653,SRS19005172,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93982,,0.07316,,0.68801,,0.48964,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28159,SRR26209693,SRX21920653,SRS19005172,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 3,GSM7812982,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812982,GSM7812982: IR t2 WT 3; Danio rerio; RNA Seq,GSM7812982 r1,GSM7812982,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A21_S38_L006_R1_001.fastq.gz,fastq,612677312.0,6066112.0,GSM7812982 r2,0:101,A:154425053;C:147379484;G:139208932;T:171653577;N:10266,101,,,,154425053,147379484,139208932,171653577,10266,SRX21920653,SRS19005172,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93954,,0.07439,,0.68945,,0.48768,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28160,SRR26209694,SRX21920653,SRS19005172,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 3,GSM7812982,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812982,GSM7812982: IR t2 WT 3; Danio rerio; RNA Seq,GSM7812982 r1,GSM7812982,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A21_S38_L007_R1_001.fastq.gz,fastq,545311221.0,5399121.0,GSM7812982 r3,0:101,A:137422024;C:131281461;G:123803444;T:152799164;N:5128,101,,,,137422024,131281461,123803444,152799164,5128,SRX21920653,SRS19005172,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94119,,0.07433,,0.6886,,0.48763,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28161,SRR26209695,SRX21920653,SRS19005172,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 3,GSM7812982,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812982,GSM7812982: IR t2 WT 3; Danio rerio; RNA Seq,GSM7812982 r1,GSM7812982,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A21_S68_L007_R1_001.fastq.gz,fastq,643233246.0,6368646.0,GSM7812982 r4,0:101,A:162062613;C:155064589;G:146625670;T:179468362;N:12012,101,,,,162062613,155064589,146625670,179468362,12012,SRX21920653,SRS19005172,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94076,,0.07335,,0.68747,,0.48953,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28162,SRR26209696,SRX21920653,SRS19005172,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 3,GSM7812982,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812982,GSM7812982: IR t2 WT 3; Danio rerio; RNA Seq,GSM7812982 r1,GSM7812982,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A21_S68_L008_R1_001.fastq.gz,fastq,643010339.0,6366439.0,GSM7812982 r5,0:101,A:161939065;C:154897858;G:146526716;T:179627762;N:18938,101,,,,161939065,154897858,146526716,179627762,18938,SRX21920653,SRS19005172,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94077,,0.07428,,0.68852,,0.4878,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28163,SRR26209697,SRX21920652,SRS19005171,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 2,GSM7812981,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812981,GSM7812981: IR t2 WT 2; Danio rerio; RNA Seq,GSM7812981 r1,GSM7812981,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A20_S37_L005_R1_001.fastq.gz,fastq,608303002.0,6022802.0,GSM7812981 r1,0:101,A:151266125;C:146608795;G:139308397;T:171114479;N:5206,101,,,,151266125,146608795,139308397,171114479,5206,SRX21920652,SRS19005171,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.9409,,0.06934,,0.68702,,0.48691,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28164,SRR26209698,SRX21920652,SRS19005171,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 2,GSM7812981,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812981,GSM7812981: IR t2 WT 2; Danio rerio; RNA Seq,GSM7812981 r1,GSM7812981,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A20_S37_L006_R1_001.fastq.gz,fastq,602278857.0,5963157.0,GSM7812981 r2,0:101,A:149885037;C:145060278;G:137831227;T:169492101;N:10214,101,,,,149885037,145060278,137831227,169492101,10214,SRX21920652,SRS19005171,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94168,,0.06967,,0.68491,,0.48684,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28165,SRR26209699,SRX21920652,SRS19005171,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 2,GSM7812981,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812981,GSM7812981: IR t2 WT 2; Danio rerio; RNA Seq,GSM7812981 r1,GSM7812981,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A20_S37_L007_R1_001.fastq.gz,fastq,539699863.0,5343563.0,GSM7812981 r3,0:101,A:134101752;C:130207416;G:123553593;T:151832349;N:4753,101,,,,134101752,130207416,123553593,151832349,4753,SRX21920652,SRS19005171,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94262,,0.06995,,0.68605,,0.48097,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28166,SRR26209700,SRX21920652,SRS19005171,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 2,GSM7812981,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812981,GSM7812981: IR t2 WT 2; Danio rerio; RNA Seq,GSM7812981 r1,GSM7812981,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A20_S13_L007_R1_001.fastq.gz,fastq,629529263.0,6232963.0,GSM7812981 r4,0:101,A:156345013;C:152106432;G:144536894;T:176529480;N:11444,101,,,,156345013,152106432,144536894,176529480,11444,SRX21920652,SRS19005171,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94267,,0.06864,,0.68477,,0.47912,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28167,SRR26209701,SRX21920652,SRS19005171,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,IR t2 WT 2,GSM7812981,,source name:whole embryo|tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR|geo loc name:missing|collection date:missing,IR t2 WT 2,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t2|genotype:WT|treatment:IR,GSM7812981,GSM7812981: IR t2 WT 2; Danio rerio; RNA Seq,GSM7812981 r1,GSM7812981,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A20_S13_L008_R1_001.fastq.gz,fastq,633828732.0,6275532.0,GSM7812981 r5,0:101,A:157411401;C:153033686;G:145422340;T:177942918;N:18387,101,,,,157411401,153033686,145422340,177942918,18387,SRX21920652,SRS19005171,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.94386,,0.06993,,0.68479,,0.48216,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28168,SRR26209702,SRX21920651,SRS19005170,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,un t1 WT 3,GSM7813000,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un|geo loc name:missing|collection date:missing,un t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un,GSM7813000,GSM7813000: un t1 WT 3; Danio rerio; RNA Seq,GSM7813000 r1,GSM7813000,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A3_S47_L005_R1_001.fastq.gz,fastq,576015423.0,5703123.0,GSM7813000 r1,0:101,A:142483427;C:134492274;G:128574929;T:170459571;N:5222,101,,,,142483427,134492274,128574929,170459571,5222,SRX21920651,SRS19005170,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93576,,0.07681,,0.6939,,0.4794,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28169,SRR26209703,SRX21920651,SRS19005170,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,un t1 WT 3,GSM7813000,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un|geo loc name:missing|collection date:missing,un t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un,GSM7813000,GSM7813000: un t1 WT 3; Danio rerio; RNA Seq,GSM7813000 r1,GSM7813000,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A3_S47_L006_R1_001.fastq.gz,fastq,568813012.0,5631812.0,GSM7813000 r2,0:101,A:140699035;C:132793802;G:126863421;T:168447319;N:9435,101,,,,140699035,132793802,126863421,168447319,9435,SRX21920651,SRS19005170,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93455,,0.07506,,0.69229,,0.47926,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28170,SRR26209704,SRX21920651,SRS19005170,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,un t1 WT 3,GSM7813000,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un|geo loc name:missing|collection date:missing,un t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un,GSM7813000,GSM7813000: un t1 WT 3; Danio rerio; RNA Seq,GSM7813000 r1,GSM7813000,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A3_S47_L007_R1_001.fastq.gz,fastq,510666908.0,5056108.0,GSM7813000 r3,0:101,A:126264547;C:119308486;G:114018656;T:151070721;N:4498,101,,,,126264547,119308486,114018656,151070721,4498,SRX21920651,SRS19005170,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93621,,0.07582,,0.6928,,0.48424,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28171,SRR26209705,SRX21920651,SRS19005170,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,un t1 WT 3,GSM7813000,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un|geo loc name:missing|collection date:missing,un t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un,GSM7813000,GSM7813000: un t1 WT 3; Danio rerio; RNA Seq,GSM7813000 r1,GSM7813000,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A3_S5_L007_R1_001.fastq.gz,fastq,602866980.0,5968980.0,GSM7813000 r4,0:101,A:148987273;C:141267314;G:134805122;T:177796181;N:11090,101,,,,148987273,141267314,134805122,177796181,11090,SRX21920651,SRS19005170,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93771,,0.07611,,0.69305,,0.48012,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures
28172,SRR26209706,SRX21920651,SRS19005170,SRP463749,PRJNA1022096,Zebrafish reveal new roles for Fam83f in hatching and DNA damage mediated autophagic responses,GSE244291,Transcriptome Analysis,The FAM83 Family with sequence similarity 83 family is highly conserved in vertebrates  yet little is known of the functions of these proteins beyond a correlation with oncogenesis. Of the family  FAM83F is of particular interest because it is the only membrane targeted FAM83 protein. FAM83F has been shown to activate the canonical Wnt signalling pathway and bind to and stabilize p53 when overexpressed  two pathways often dysregulated in disease.  Insights into gene function can often be gained by studying the roles they play during development  and here we report the generation of fam83f knock out fam83f /  zebrafish  which we have used to elucidate the role of Fam83f in vivo. We show that endogenous fam83f is most strongly expressed in the proteolytic enzyme containing hatch gland of developing zebrafish embryos  and that fam83f /  embryos hatch earlier than WT counterparts  despite developing at a comparable temporal rate. We demonstrate that fam83f /  embryos are more sensitive to ionizing radiation than WT embryos  a finding that contrasts with the previously reported role of FAM83F as a stabilizer of p53. Transcriptomic analysis shows that loss of fam83f causes downregulation of phosphatidylinositol 3 phosphate PI3P binding proteins and impairment of cellular degradation pathways  particularly autophagy  which is a crucial component of the DNA damage response. Finally  we show that Fam83f protein is itself targeted to the lysosome when expressed in cultured cells  and that this localization is dependent upon a C' terminal signal sequence.  The zebrafish lines we have generated here suggest for the first time that Fam83f plays an important role in autophagic/lysosomal processes  resulting in dysregulated hatching and increased sensitivity to genotoxic stress in vivo. Overall design: fam83fa /  zebrafish are more sensitive to ionizing radiation IR than WT counterparts. We conducted bulk RNA seq on WT vs two different fam83fa /  K1 and K2 zebrafish lines by subjecting 24 hpf embryos from each genotype to IR then extracting total RNA at 2 and 10 hours following treament t1 and t2.  Three biological replicates of a minimum of 10 embryos per replicate were sequenced by bulk RNA seq to to identify any differences in the DNA damage response between WT and fam83fa /  mutants. Treatments: AD = Actinomycin D in DMSO vehicle IR = ionizing radiation 20 Grays gamma radiation unDMSO = untreated AD control vehicle only i.e. DMSO un = untreated IR control,,pubmed:39437839,,un t1 WT 3,GSM7813000,,source name:whole embryo|tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un|geo loc name:missing|collection date:missing,un t1 WT 3,Cutadapt  1.9.1 rsem 1.3.0 star 2.5.2a Assembly: GRCz11 assembly Supplementary files format and content: *.genes.results are rsem count files,whole embryo,Embryos were exposed to gamma IR of 20 Gy at xxx hpf,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,Zebrafish embryos post collection were maintained at 28.5C in E2 medium at a density ⋜  50 embryos,tissue:whole embryo|timepoint:t1|genotype:WT|treatment:un,GSM7813000,GSM7813000: un t1 WT 3; Danio rerio; RNA Seq,GSM7813000 r1,GSM7813000,1,Total RNA was extracted using RNeasy Mini Kit QIAGEN rRNA depletion Rio Zero Plus rRNA Depletion Kit Ilumina  then library prep using KAPA mRNA HyperPrep Kit for Ilumina Platforms,,RNA-Seq,TRANSCRIPTOMIC,cDNA,SINGLE,ILLUMINA,Illumina HiSeq 4000,,SRP463749,,loader:fastq load.py,JON686A3_S5_L008_R1_001.fastq.gz,fastq,605447934.0,5994534.0,GSM7813000 r5,0:101,A:149696103;C:141763945;G:135323063;T:178646888;N:17935,101,,,,149696103,141763945,135323063,178646888,17935,SRX21920651,SRS19005170,SRA1722794,"Devenport, Molecular Biology, Princeton University","Devenport, Molecular Biology, Princeton University",1,0.93786,,0.0763,,0.6911,,0.48344,,101,,B,,usable mapping rate,illumina,hiseq_era,unknown,rrna_depletion,unknown,bulk,bulk,bulk,,United States,2023-09-28,Undetermined,Embryo,Whole Organism,All anatomical structures