RNAquarium Metadata Server
Institute Website Terms of Use Privacy Policy

run_metadata

294 rows where devstage_curation_coarse = "Undetermined" and technology = "bulk"

✎ View and edit SQL

This data as json, CSV (advanced)

tissue_curation 9

experiment.library_selection 5

experiment.library_layout 2

technology 1

  • bulk · 294 ✖

experiment.platform 1

experiment.library_strategy 1

experiment.library_source 1

devstage_curation_coarse 1

  • Undetermined · 294 ✖

devstage_curation 1

Link 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
10391 10391 ERR8516975 ERX8083451 ERS10521298 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Sibling neurite SAMEA12922152 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922152|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Sibling neurite|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq sibling +/+ and +/ |growth condition:transwell culture|organism part:neurite|sample name:E MTAB 11431:Sibling neurite                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Sibling neurite p Sibling neurite p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq sibling +/+ and +/ |Experimental Factor: organism part:neurite RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X4_190227_A00421_38_AH7523DRXX_S56_R1_001.fastq.gz 15812X4_190227_A00421_38_AH7523DRXX_S56_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X4 190227 A00421 38 AH7523DRXX S56 R 0:51 1:51 A:1077092958;C:949537387;G:955020348;T:1099432979;N:20556852 51 51     1077092958 949537387 955020348 1099432979 20556852 ERX8083451 ERS10521298 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.9053 0.9259 0.21658 0.22155 0.69369 0.69179 0.50726 0.50871 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10392 10392 ERR8516976 ERX8083451 ERS10521298 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Sibling neurite SAMEA12922152 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922152|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Sibling neurite|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq sibling +/+ and +/ |growth condition:transwell culture|organism part:neurite|sample name:E MTAB 11431:Sibling neurite                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Sibling neurite p Sibling neurite p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq sibling +/+ and +/ |Experimental Factor: organism part:neurite RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X5_190227_A00421_38_AH7523DRXX_S55_R1_001.fastq.gz 15812X5_190227_A00421_38_AH7523DRXX_S55_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X5 190227 A00421 38 AH7523DRXX S55 R 0:51 1:51 A:972081222;C:890179393;G:888655698;T:998443264;N:18934747 51 51     972081222 890179393 888655698 998443264 18934747 ERX8083451 ERS10521298 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.86107 0.87807 0.22063 0.23029 0.70859 0.70561 0.51656 0.51946 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10393 10393 ERR8516977 ERX8083451 ERS10521298 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Sibling neurite SAMEA12922152 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922152|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Sibling neurite|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq sibling +/+ and +/ |growth condition:transwell culture|organism part:neurite|sample name:E MTAB 11431:Sibling neurite                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Sibling neurite p Sibling neurite p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq sibling +/+ and +/ |Experimental Factor: organism part:neurite RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X6_190227_A00421_38_AH7523DRXX_S54_R1_001.fastq.gz 15812X6_190227_A00421_38_AH7523DRXX_S54_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X6 190227 A00421 38 AH7523DRXX S54 R 0:51 1:51 A:728798881;C:962223604;G:958876331;T:735449513;N:17094231 51 51     728798881 962223604 958876331 735449513 17094231 ERX8083451 ERS10521298 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.54616 0.55881 0.13313 0.14036 0.84295 0.84185 0.64193 0.59762 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10394 10394 ERR8516972 ERX8083450 ERS10521297 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Sibling cellular SAMEA12922151 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922151|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Sibling cellular|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq sibling +/+ and +/ |growth condition:transwell culture|organism part:neuron|sample name:E MTAB 11431:Sibling cellular                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Sibling cellular p Sibling cellular p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq sibling +/+ and +/ |Experimental Factor: organism part:neuron RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X1_190227_A00421_38_AH7523DRXX_S59_R1_001.fastq.gz 15812X1_190227_A00421_38_AH7523DRXX_S59_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X1 190227 A00421 38 AH7523DRXX S59 R 0:51 1:51 A:837274632;C:1062368015;G:1049892288;T:853310517;N:19213786 51 51     837274632 1062368015 1049892288 853310517 19213786 ERX8083450 ERS10521297 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.5726 0.57788 0.13781 0.14082 0.80616 0.80452 0.61581 0.60389 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10395 10395 ERR8516973 ERX8083450 ERS10521297 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Sibling cellular SAMEA12922151 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922151|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Sibling cellular|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq sibling +/+ and +/ |growth condition:transwell culture|organism part:neuron|sample name:E MTAB 11431:Sibling cellular                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Sibling cellular p Sibling cellular p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq sibling +/+ and +/ |Experimental Factor: organism part:neuron RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X2_190227_A00421_38_AH7523DRXX_S58_R1_001.fastq.gz 15812X2_190227_A00421_38_AH7523DRXX_S58_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X2 190227 A00421 38 AH7523DRXX S58 R 0:51 1:51 A:897813231;C:796012893;G:794839496;T:923696030;N:17221274 51 51     897813231 796012893 794839496 923696030 17221274 ERX8083450 ERS10521297 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.92095 0.94156 0.18892 0.20024 0.6901 0.68905 0.49377 0.50086 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10396 10396 ERR8516974 ERX8083450 ERS10521297 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Sibling cellular SAMEA12922151 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922151|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Sibling cellular|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq sibling +/+ and +/ |growth condition:transwell culture|organism part:neuron|sample name:E MTAB 11431:Sibling cellular                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Sibling cellular p Sibling cellular p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq sibling +/+ and +/ |Experimental Factor: organism part:neuron RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X3_190227_A00421_38_AH7523DRXX_S57_R1_001.fastq.gz 15812X3_190227_A00421_38_AH7523DRXX_S57_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X3 190227 A00421 38 AH7523DRXX S57 R 0:51 1:51 A:951912827;C:1107150666;G:1086060798;T:973791571;N:20785248 51 51     951912827 1107150666 1086060798 973791571 20785248 ERX8083450 ERS10521297 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.63792 0.62667 0.18547 0.18671 0.78756 0.78549 0.59274 0.55478 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10397 10397 ERR8516969 ERX8083449 ERS10521296 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Null neurite SAMEA12922150 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922150|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Null neurite|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq null / |growth condition:transwell culture|organism part:neurite|sample name:E MTAB 11431:Null neurite                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Null neurite p Null neurite p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq null / |Experimental Factor: organism part:neurite RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X10_190227_A00421_38_AH7523DRXX_S48_R1_001.fastq.gz 15812X10_190227_A00421_38_AH7523DRXX_S48_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X10 190227 A00421 38 AH7523DRXX S48 R 0:51 1:51 A:925784769;C:934445856;G:959155668;T:924080408;N:18878983 51 51     925784769 934445856 959155668 924080408 18878983 ERX8083449 ERS10521296 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.59503 0.61112 0.1947 0.20225 0.76512 0.76337 0.54584 0.54345 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10398 10398 ERR8516970 ERX8083449 ERS10521296 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Null neurite SAMEA12922150 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922150|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Null neurite|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq null / |growth condition:transwell culture|organism part:neurite|sample name:E MTAB 11431:Null neurite                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Null neurite p Null neurite p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq null / |Experimental Factor: organism part:neurite RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X11_190227_A00421_38_AH7523DRXX_S52_R1_001.fastq.gz 15812X11_190227_A00421_38_AH7523DRXX_S52_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X11 190227 A00421 38 AH7523DRXX S52 R 0:51 1:51 A:991755033;C:864808531;G:892202564;T:992188806;N:18881958 51 51     991755033 864808531 892202564 992188806 18881958 ERX8083449 ERS10521296 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.86612 0.88689 0.26181 0.2728 0.7094 0.7091 0.53639 0.53906 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10399 10399 ERR8516971 ERX8083449 ERS10521296 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Null neurite SAMEA12922150 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922150|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Null neurite|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq null / |growth condition:transwell culture|organism part:neurite|sample name:E MTAB 11431:Null neurite                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Null neurite p Null neurite p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq null / |Experimental Factor: organism part:neurite RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X12_190227_A00421_38_AH7523DRXX_S50_R1_001.fastq.gz 15812X12_190227_A00421_38_AH7523DRXX_S50_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X12 190227 A00421 38 AH7523DRXX S50 R 0:51 1:51 A:766707527;C:798667604;G:818782599;T:773280942;N:15938306 51 51     766707527 798667604 818782599 773280942 15938306 ERX8083449 ERS10521296 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.88811 0.92834 0.21869 0.22669 0.72878 0.72604 0.55598 0.57831 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10400 10400 ERR8516966 ERX8083448 ERS10521295 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Null cellular SAMEA12922149 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922149|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Null cellular|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq null / |growth condition:transwell culture|organism part:neuron|sample name:E MTAB 11431:Null cellular                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Null cellular p Null cellular p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq null / |Experimental Factor: organism part:neuron RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X7_190227_A00421_38_AH7523DRXX_S53_R1_001.fastq.gz 15812X7_190227_A00421_38_AH7523DRXX_S53_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X7 190227 A00421 38 AH7523DRXX S53 R 0:51 1:51 A:774360373;C:720215184;G:719479745;T:796239200;N:15182374 51 51     774360373 720215184 719479745 796239200 15182374 ERX8083448 ERS10521295 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.79643 0.81194 0.25554 0.2603 0.72236 0.72021 0.51775 0.51678 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10401 10401 ERR8516967 ERX8083448 ERS10521295 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Null cellular SAMEA12922149 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922149|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Null cellular|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq null / |growth condition:transwell culture|organism part:neuron|sample name:E MTAB 11431:Null cellular                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Null cellular p Null cellular p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq null / |Experimental Factor: organism part:neuron RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X8_190227_A00421_38_AH7523DRXX_S51_R1_001.fastq.gz 15812X8_190227_A00421_38_AH7523DRXX_S51_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X8 190227 A00421 38 AH7523DRXX S51 R 0:51 1:51 A:739921027;C:667375549;G:663864111;T:764302396;N:14288091 51 51     739921027 667375549 663864111 764302396 14288091 ERX8083448 ERS10521295 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.90817 0.92909 0.23387 0.24814 0.70088 0.69842 0.51238 0.51267 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
10402 10402 ERR8516968 ERX8083448 ERS10521295 ERP135383 PRJEB50776 Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E-MTAB-11431 Other Zebrafish primary neurons either sfpq sibling/control +/+ +/ or null / were cultured in transwell inserts. At DIV2 for each genotype cellular and neurite tissues were separately isolated RNA extracted and total RNAseq performed. ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19   Protocols: Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Null cellular SAMEA12922149 Centre for Developmental Neurobiology, King's College London ENA first public:2022 02 19|ENA last update:2022 02 19|External Id:SAMEA12922149|INSDC center alias:Centre for Developmental Neurobiology King's College London|INSDC center name:Centre for Developmental Neurobiology King's College London|INSDC first public:2022 02 19T00:15:43Z|INSDC last update:2022 02 19T00:15:43Z|INSDC status:public|Submitter Id:E MTAB 11431:Null cellular|broker name:ArrayExpress|common name:zebrafish|genotype:sfpq null / |growth condition:transwell culture|organism part:neuron|sample name:E MTAB 11431:Null cellular                 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue E MTAB 11431:Null cellular p Null cellular p Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue Cellular and neurite tissues cultured in transwell inserts were collected separately. Cellular tissue by swabbing and neurite tissue using a cell scraper Qiagen RNeasy Micro Kit TruSeq Stranded Total RNA Library Prep Gold kit with Ribo Zero Gold depleteion Experimental Factor: genotype:sfpq null / |Experimental Factor: organism part:neuron RNA-Seq TRANSCRIPTOMIC RANDOM PAIRED ILLUMINA Illumina NovaSeq 6000   ERP135383 Illumina NovaSeq 6000 paired end sequencing; Total RNAseq of sfpq sibling +/+ +/ and null / primary zebrafish neuron cellular and neurite tissue ENA FIRST PUBLIC:2022 02 19|ENA LAST UPDATE:2022 02 19|loader:fastq load.py 15812X9_190227_A00421_38_AH7523DRXX_S49_R1_001.fastq.gz 15812X9_190227_A00421_38_AH7523DRXX_S49_R2_001.fastq.gz fastq fastq     E MTAB 11431:15812X9 190227 A00421 38 AH7523DRXX S49 R 0:51 1:51 A:882831441;C:935213418;G:957033335;T:879085993;N:18444957 51 51     882831441 935213418 957033335 879085993 18444957 ERX8083448 ERS10521295 ERA8932807 Centre for Developmental Neurobiology, King Centre for Developmental Neurobiology, King 2 0.76218 0.7682 0.18357 0.18521 0.74444 0.74272 0.46714 0.55518 51 51 B B biological fallback assumption illumina novaseq_era unknown random_priming ribozero bulk bulk bulk   United Kingdom 2022-02-19 Undetermined Undetermined Brain Nervous System
30556 30556 SRR27836071 SRX23499420 SRS20351177 SRP487485 PRJNA1072072 Rbpms2 promotes female fate upstream of the nutrient sensing Gator2 complex component Mios GSE254850 Transcriptome Analysis Reproductive success relies on proper establishment and maintenance of biological sex. In many animals including mammals the primary gonad is initially ovary in character. We previously showed the RNA binding protein RNAbp Rbpms2 is required for ovary fate in zebrafish. Here we identified Rbpms2 targets in oocytesRbpms2 bound oocyte RNAs; rboRNAs. We identify Rbpms2 as a translational regulator ofrboRNAs which include testis factors and ribosome biogenesis factors. Further genetic analyses indicate that Rbpms2 promotes nucleolar amplification via the mTorc1 signaling pathway specifically through the mTorc1 activating Gap activity towards Rags 2 Gator2 component Missing oocyte Mios. Cumulatively our findings indicate that early gonocytes are in a dual poised bipotential state in which Rbpms2 acts as a binary fate switch. Specifically Rbpms2 represses testis factors and promotes oocyte factors to promote oocyte progression through an essential Gator2 mediated checkpoint thereby integrating regulation of sexual differentiation factors and nutritional availability pathways in zebrafish oogenesis. Overall design: To determine the RNA targets of Rbpms2 we generated wildtype female zebrafish expressing Rbpms2 mApple or mApple alone fusion proteins exclusively in the germline. Immunoprecipitation was performed in 2 adult female ovaries per transgene. Crosslinked and uncrosslinked samples for Rbpms2 mApple expressing fish and crosslined and uncrosslinked samples for mApple expressing fish were sequenced. RNAs found in the Rbpms2 mApple crosslinked and the mApple crosslinked and uncrosslinked datasets that were also present in the Rbpms2 mApple uncrosslinked dataset were excluded. RNAs present only in the uncrosslinked datasets were counted as RNA targets of Rbpms2. To characterize the transcriptional differences of rbpms2 mutants vs wildtype fish prior to sex determination 21 dpf we performed bulk RNA sequencing on n=3 dpf 21 dpf wildtype and n=3 rbpms2 mutant fish. DESeq was then performed for Differential…   pubmed:38898112   Rbpms2 mApple crosslinked SR3 GSM8059038   source name:Gonad|tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype|geo loc name:missing|collection date:missing Rbpms2 mApple crosslinked SR3 Basespace illumina platform was used and reads were mapped using tophate2 aligner. Estimation of reference genes and transcript was done using cufflinks and reads were mapped to the genome GRCz10. Reads were aligned with the TopHat Alignment App. GRCz10 CSV file that compiled includes tracking ids gene loci and FPKMs for each samples CSV files include tracking and gene id gene short name tss id locus and FPKM for each sample Gonad   RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype GSM8059038 GSM8059038: Rbpms2 mApple crosslinked SR3; Danio rerio; RNA Seq GSM8059038 r1 GSM8059038 1 RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP487485     SR-3_S4_L001_R1_001.fastq.gz SR-3_S4_L001_R2_001.fastq.gz fastq fastq 588252864.0 3949222.0 GSM8059038 r1 0:74.42 1:74.53 A:116383167;C:176622592;G:176850622;T:118306997;N:89486 74 74     116383167 176622592 176850622 118306997 89486 SRX23499420 SRS20351177 SRA1796363 Marlow, CDRB, Icahn School of Medicine Mount Sinai Marlow, CDRB, Icahn School of Medicine Mount Sinai                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified trueseq bulk bulk bulk   United States 2024-02-01 Undetermined Undetermined Gonad Reproductive System
30557 30557 SRR27836072 SRX23499419 SRS20351178 SRP487485 PRJNA1072072 Rbpms2 promotes female fate upstream of the nutrient sensing Gator2 complex component Mios GSE254850 Transcriptome Analysis Reproductive success relies on proper establishment and maintenance of biological sex. In many animals including mammals the primary gonad is initially ovary in character. We previously showed the RNA binding protein RNAbp Rbpms2 is required for ovary fate in zebrafish. Here we identified Rbpms2 targets in oocytesRbpms2 bound oocyte RNAs; rboRNAs. We identify Rbpms2 as a translational regulator ofrboRNAs which include testis factors and ribosome biogenesis factors. Further genetic analyses indicate that Rbpms2 promotes nucleolar amplification via the mTorc1 signaling pathway specifically through the mTorc1 activating Gap activity towards Rags 2 Gator2 component Missing oocyte Mios. Cumulatively our findings indicate that early gonocytes are in a dual poised bipotential state in which Rbpms2 acts as a binary fate switch. Specifically Rbpms2 represses testis factors and promotes oocyte factors to promote oocyte progression through an essential Gator2 mediated checkpoint thereby integrating regulation of sexual differentiation factors and nutritional availability pathways in zebrafish oogenesis. Overall design: To determine the RNA targets of Rbpms2 we generated wildtype female zebrafish expressing Rbpms2 mApple or mApple alone fusion proteins exclusively in the germline. Immunoprecipitation was performed in 2 adult female ovaries per transgene. Crosslinked and uncrosslinked samples for Rbpms2 mApple expressing fish and crosslined and uncrosslinked samples for mApple expressing fish were sequenced. RNAs found in the Rbpms2 mApple crosslinked and the mApple crosslinked and uncrosslinked datasets that were also present in the Rbpms2 mApple uncrosslinked dataset were excluded. RNAs present only in the uncrosslinked datasets were counted as RNA targets of Rbpms2. To characterize the transcriptional differences of rbpms2 mutants vs wildtype fish prior to sex determination 21 dpf we performed bulk RNA sequencing on n=3 dpf 21 dpf wildtype and n=3 rbpms2 mutant fish. DESeq was then performed for Differential…   pubmed:38898112   Rbpms2 mApple uncrosslinked SR2 GSM8059037   source name:Gonad|tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype|geo loc name:missing|collection date:missing Rbpms2 mApple uncrosslinked SR2 Basespace illumina platform was used and reads were mapped using tophate2 aligner. Estimation of reference genes and transcript was done using cufflinks and reads were mapped to the genome GRCz10. Reads were aligned with the TopHat Alignment App. GRCz10 CSV file that compiled includes tracking ids gene loci and FPKMs for each samples CSV files include tracking and gene id gene short name tss id locus and FPKM for each sample Gonad   RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype GSM8059037 GSM8059037: Rbpms2 mApple uncrosslinked SR2; Danio rerio; RNA Seq GSM8059037 r1 GSM8059037 1 RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP487485     SR-2_S3_L001_R1_001.fastq.gz SR-2_S3_L001_R2_001.fastq.gz fastq fastq 547329260.0 3670350.0 GSM8059037 r1 0:74.51 1:74.61 A:109193152;C:163365002;G:162344228;T:112378069;N:48809 74 74     109193152 163365002 162344228 112378069 48809 SRX23499419 SRS20351178 SRA1796363 Marlow, CDRB, Icahn School of Medicine Mount Sinai Marlow, CDRB, Icahn School of Medicine Mount Sinai                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified trueseq bulk bulk bulk   United States 2024-02-01 Undetermined Undetermined Gonad Reproductive System
30558 30558 SRR27836073 SRX23499418 SRS20351176 SRP487485 PRJNA1072072 Rbpms2 promotes female fate upstream of the nutrient sensing Gator2 complex component Mios GSE254850 Transcriptome Analysis Reproductive success relies on proper establishment and maintenance of biological sex. In many animals including mammals the primary gonad is initially ovary in character. We previously showed the RNA binding protein RNAbp Rbpms2 is required for ovary fate in zebrafish. Here we identified Rbpms2 targets in oocytesRbpms2 bound oocyte RNAs; rboRNAs. We identify Rbpms2 as a translational regulator ofrboRNAs which include testis factors and ribosome biogenesis factors. Further genetic analyses indicate that Rbpms2 promotes nucleolar amplification via the mTorc1 signaling pathway specifically through the mTorc1 activating Gap activity towards Rags 2 Gator2 component Missing oocyte Mios. Cumulatively our findings indicate that early gonocytes are in a dual poised bipotential state in which Rbpms2 acts as a binary fate switch. Specifically Rbpms2 represses testis factors and promotes oocyte factors to promote oocyte progression through an essential Gator2 mediated checkpoint thereby integrating regulation of sexual differentiation factors and nutritional availability pathways in zebrafish oogenesis. Overall design: To determine the RNA targets of Rbpms2 we generated wildtype female zebrafish expressing Rbpms2 mApple or mApple alone fusion proteins exclusively in the germline. Immunoprecipitation was performed in 2 adult female ovaries per transgene. Crosslinked and uncrosslinked samples for Rbpms2 mApple expressing fish and crosslined and uncrosslinked samples for mApple expressing fish were sequenced. RNAs found in the Rbpms2 mApple crosslinked and the mApple crosslinked and uncrosslinked datasets that were also present in the Rbpms2 mApple uncrosslinked dataset were excluded. RNAs present only in the uncrosslinked datasets were counted as RNA targets of Rbpms2. To characterize the transcriptional differences of rbpms2 mutants vs wildtype fish prior to sex determination 21 dpf we performed bulk RNA sequencing on n=3 dpf 21 dpf wildtype and n=3 rbpms2 mutant fish. DESeq was then performed for Differential…   pubmed:38898112   mApple control crosslinked SR8 GSM8059036   source name:Gonad|tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype|geo loc name:missing|collection date:missing mApple control crosslinked SR8 Basespace illumina platform was used and reads were mapped using tophate2 aligner. Estimation of reference genes and transcript was done using cufflinks and reads were mapped to the genome GRCz10. Reads were aligned with the TopHat Alignment App. GRCz10 CSV file that compiled includes tracking ids gene loci and FPKMs for each samples CSV files include tracking and gene id gene short name tss id locus and FPKM for each sample Gonad   RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype GSM8059036 GSM8059036: mApple control crosslinked SR8; Danio rerio; RNA Seq GSM8059036 r1 GSM8059036 1 RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP487485     SR-8_S6_L001_R1_001.fastq.gz SR-8_S6_L001_R2_001.fastq.gz fastq fastq 474378287.0 3180744.0 GSM8059036 r1 0:74.52 1:74.62 A:90310344;C:145884340;G:146185172;T:91942086;N:56345 74 74     90310344 145884340 146185172 91942086 56345 SRX23499418 SRS20351176 SRA1796363 Marlow, CDRB, Icahn School of Medicine Mount Sinai Marlow, CDRB, Icahn School of Medicine Mount Sinai                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified trueseq bulk bulk bulk   United States 2024-02-01 Undetermined Undetermined Gonad Reproductive System
30559 30559 SRR27836074 SRX23499417 SRS20351175 SRP487485 PRJNA1072072 Rbpms2 promotes female fate upstream of the nutrient sensing Gator2 complex component Mios GSE254850 Transcriptome Analysis Reproductive success relies on proper establishment and maintenance of biological sex. In many animals including mammals the primary gonad is initially ovary in character. We previously showed the RNA binding protein RNAbp Rbpms2 is required for ovary fate in zebrafish. Here we identified Rbpms2 targets in oocytesRbpms2 bound oocyte RNAs; rboRNAs. We identify Rbpms2 as a translational regulator ofrboRNAs which include testis factors and ribosome biogenesis factors. Further genetic analyses indicate that Rbpms2 promotes nucleolar amplification via the mTorc1 signaling pathway specifically through the mTorc1 activating Gap activity towards Rags 2 Gator2 component Missing oocyte Mios. Cumulatively our findings indicate that early gonocytes are in a dual poised bipotential state in which Rbpms2 acts as a binary fate switch. Specifically Rbpms2 represses testis factors and promotes oocyte factors to promote oocyte progression through an essential Gator2 mediated checkpoint thereby integrating regulation of sexual differentiation factors and nutritional availability pathways in zebrafish oogenesis. Overall design: To determine the RNA targets of Rbpms2 we generated wildtype female zebrafish expressing Rbpms2 mApple or mApple alone fusion proteins exclusively in the germline. Immunoprecipitation was performed in 2 adult female ovaries per transgene. Crosslinked and uncrosslinked samples for Rbpms2 mApple expressing fish and crosslined and uncrosslinked samples for mApple expressing fish were sequenced. RNAs found in the Rbpms2 mApple crosslinked and the mApple crosslinked and uncrosslinked datasets that were also present in the Rbpms2 mApple uncrosslinked dataset were excluded. RNAs present only in the uncrosslinked datasets were counted as RNA targets of Rbpms2. To characterize the transcriptional differences of rbpms2 mutants vs wildtype fish prior to sex determination 21 dpf we performed bulk RNA sequencing on n=3 dpf 21 dpf wildtype and n=3 rbpms2 mutant fish. DESeq was then performed for Differential…   pubmed:38898112   mApple control uncrosslinked SR6 GSM8059035   source name:Gonad|tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype|geo loc name:missing|collection date:missing mApple control uncrosslinked SR6 Basespace illumina platform was used and reads were mapped using tophate2 aligner. Estimation of reference genes and transcript was done using cufflinks and reads were mapped to the genome GRCz10. Reads were aligned with the TopHat Alignment App. GRCz10 CSV file that compiled includes tracking ids gene loci and FPKMs for each samples CSV files include tracking and gene id gene short name tss id locus and FPKM for each sample Gonad   RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   tissue:Gonad|cell type:Germline and somatic|genotype:Wildtype GSM8059035 GSM8059035: mApple control uncrosslinked SR6; Danio rerio; RNA Seq GSM8059035 r1 GSM8059035 1 RNA was extracted with an Rneasy Mini Kit Qiagen 74104 Libraries were generated with an Illumina Truseq RNA Library Prep kit Illumina 20020589   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP487485     SR-6_S5_L001_R1_001.fastq.gz SR-6_S5_L001_R2_001.fastq.gz fastq fastq 1667210566.0 11187841.0 GSM8059035 r1 0:74.46 1:74.56 A:348153529;C:480420209;G:474792496;T:363567978;N:276354 74 74     348153529 480420209 474792496 363567978 276354 SRX23499417 SRS20351175 SRA1796363 Marlow, CDRB, Icahn School of Medicine Mount Sinai Marlow, CDRB, Icahn School of Medicine Mount Sinai                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified trueseq bulk bulk bulk   United States 2024-02-01 Undetermined Undetermined Gonad Reproductive System
31502 31502 SRR28411462 SRX24015869 SRS20810998 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88+/+ 24 hpci 2 GSM8159071   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88+/+ 24 hpci 2 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury GSM8159071 GSM8159071: injured tissue myd88+/+ 24 hpci 2; Danio rerio; RNA Seq GSM8159071 r1 GSM8159071 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_WT2_24h_pci_R1.fastq.gz fastq 2454645976.0 33159360.0 GSM8159071 r1 0:74.03 A:660213492;C:527347733;G:572126573;T:694765347;N:192831 74       660213492 527347733 572126573 694765347 192831 SRX24015869 SRS20810998 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31503 31503 SRR28411463 SRX24015868 SRS20810997 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88+/+ 1 hpci 2 GSM8159070   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88+/+ 1 hpci 2 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury GSM8159070 GSM8159070: injured tissue myd88+/+ 1 hpci 2; Danio rerio; RNA Seq GSM8159070 r1 GSM8159070 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_WT2_1h_pci_R1.fastq.gz fastq 2674654542.0 36003719.0 GSM8159070 r1 0:74.29 A:713621237;C:556223861;G:630990745;T:773686189;N:132510 74       713621237 556223861 630990745 773686189 132510 SRX24015868 SRS20810997 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31504 31504 SRR28411464 SRX24015867 SRS20810996 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   ventricle myd88+/+ untouched 2 GSM8159069   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment: |geo loc name:missing|collection date:missing ventricle myd88+/+ untouched 2 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment: GSM8159069 GSM8159069: ventricle myd88+/+ untouched 2; Danio rerio; RNA Seq GSM8159069 r1 GSM8159069 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_WT2_0h_pci_R1.fastq.gz fastq 2092632406.0 28163739.0 GSM8159069 r1 0:74.30 A:560190602;C:446185315;G:485011548;T:601082958;N:161983 74       560190602 446185315 485011548 601082958 161983 SRX24015867 SRS20810996 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31505 31505 SRR28411465 SRX24015866 SRS20810995 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88+/+ 24 hpci 1 GSM8159068   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88+/+ 24 hpci 1 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury GSM8159068 GSM8159068: injured tissue myd88+/+ 24 hpci 1; Danio rerio; RNA Seq GSM8159068 r1 GSM8159068 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_WT1_24h_pci_R1.fastq.gz fastq 1060148110.0 14341826.0 GSM8159068 r1 0:73.92 A:290655996;C:222128471;G:247491826;T:299784598;N:87219 73       290655996 222128471 247491826 299784598 87219 SRX24015866 SRS20810995 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31506 31506 SRR28411466 SRX24015865 SRS20810994 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88+/+ 1 hpci 1 GSM8159067   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88+/+ 1 hpci 1 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment:cardiac cryoinjury GSM8159067 GSM8159067: injured tissue myd88+/+ 1 hpci 1; Danio rerio; RNA Seq GSM8159067 r1 GSM8159067 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_WT1_1h_pci_R1.fastq.gz fastq 2594786024.0 34913792.0 GSM8159067 r1 0:74.32 A:689702458;C:551265040;G:603307580;T:750425733;N:85213 74       689702458 551265040 603307580 750425733 85213 SRX24015865 SRS20810994 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31507 31507 SRR28411467 SRX24015864 SRS20810993 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   ventricle myd88+/+ untouched 1 GSM8159066   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment: |geo loc name:missing|collection date:missing ventricle myd88+/+ untouched 1 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88+/+|treatment: GSM8159066 GSM8159066: ventricle myd88+/+ untouched 1; Danio rerio; RNA Seq GSM8159066 r1 GSM8159066 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_WT1_0h_pci_R1.fastq.gz fastq 2123516005.0 28595227.0 GSM8159066 r1 0:74.26 A:562046544;C:458761205;G:496224794;T:606313940;N:169522 74       562046544 458761205 496224794 606313940 169522 SRX24015864 SRS20810993 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31508 31508 SRR28411468 SRX24015863 SRS20810992 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88 / 24 hpci 2 GSM8159065   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88 / 24 hpci 2 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury GSM8159065 GSM8159065: injured tissue myd88 / 24 hpci 2; Danio rerio; RNA Seq GSM8159065 r1 GSM8159065 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_Homo2_24h_pci_R1.fastq.gz fastq 2509143345.0 33915175.0 GSM8159065 r1 0:73.98 A:669128241;C:547606289;G:587771598;T:704439682;N:197535 73       669128241 547606289 587771598 704439682 197535 SRX24015863 SRS20810992 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31509 31509 SRR28411469 SRX24015862 SRS20810991 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88 / 1 hpci 2 GSM8159064   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88 / 1 hpci 2 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury GSM8159064 GSM8159064: injured tissue myd88 / 1 hpci 2; Danio rerio; RNA Seq GSM8159064 r1 GSM8159064 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_Homo2_1h_pci_R1.fastq.gz fastq 2584847185.0 34784917.0 GSM8159064 r1 0:74.31 A:690941775;C:542509296;G:605002938;T:746301098;N:92078 74       690941775 542509296 605002938 746301098 92078 SRX24015862 SRS20810991 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31510 31510 SRR28411470 SRX24015861 SRS20810990 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   ventricle myd88 / untouched 2 GSM8159063   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment: |geo loc name:missing|collection date:missing ventricle myd88 / untouched 2 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment: GSM8159063 GSM8159063: ventricle myd88 / untouched 2; Danio rerio; RNA Seq GSM8159063 r1 GSM8159063 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_Homo2_0h_pci_R1.fastq.gz fastq 2178164776.0 29313471.0 GSM8159063 r1 0:74.31 A:588370831;C:457110464;G:507924919;T:624586577;N:171985 74       588370831 457110464 507924919 624586577 171985 SRX24015861 SRS20810990 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31511 31511 SRR28411471 SRX24015860 SRS20810989 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88 / 24 hpci 1 GSM8159062   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88 / 24 hpci 1 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury GSM8159062 GSM8159062: injured tissue myd88 / 24 hpci 1; Danio rerio; RNA Seq GSM8159062 r1 GSM8159062 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_Homo1_24h_pci_R1.fastq.gz fastq 2323298254.0 31332951.0 GSM8159062 r1 0:74.15 A:621931320;C:501998000;G:541224122;T:657957821;N:186991 74       621931320 501998000 541224122 657957821 186991 SRX24015860 SRS20810989 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31512 31512 SRR28411472 SRX24015859 SRS20810988 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   injured tissue myd88 / 1 hpci 1 GSM8159061   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing injured tissue myd88 / 1 hpci 1 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment:cardiac cryoinjury GSM8159061 GSM8159061: injured tissue myd88 / 1 hpci 1; Danio rerio; RNA Seq GSM8159061 r1 GSM8159061 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_Homo1_1h_pci_R1.fastq.gz fastq 2585736865.0 34790236.0 GSM8159061 r1 0:74.32 A:679380332;C:554919862;G:604907160;T:746451941;N:77570 74       679380332 554919862 604907160 746451941 77570 SRX24015859 SRS20810988 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
31513 31513 SRR28411473 SRX24015858 SRS20810987 SRP497025 PRJNA1090509 The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration dst139 GSE262169 Transcriptome Analysis The innate immune response is triggered xxx post injury and its spatiotemporal dynamics are critical for regeneration but many questions remain about its exact role. Here we show that MyD88 a key component of the innate immune response controls not only the inflammatory but also the fibrotic response during zebrafish cardiac regeneration. We find in cryoinjured myd88 / ventricles a significant reduction in neutrophil and macrophage numbers as well as the expansion of a collagen rich endocardial population. Further analyses reveal compromised PI3K/AKT pathway activation in the myd88 / endocardium and increased myofibroblasts and scarring. Notably endothelial specific overexpression of myd88 reverses these neutrophil fibrotic and scarring phenotypes. Mechanistically we identify the endocardial derived chemokine gene cxcl18b as a target of the MyD88 signaling pathway and using loss and gain of function tools show that it controls neutrophil recruitment. Altogether these findings shed light on the pivotal role of MyD88 in modulating inflammation and fibrosis during tissue regeneration. Overall design: RNA was isolated from myd88+/+ and myd88 / untouched ventricles and cryoinjured tissues at 1 and 24 hours post cryoinjury hpci and analyzed using bulk RNA sequencing parent bioproject:PRJNA1090894 pubmed:39271818   ventricle myd88 / untouched 1 GSM8159060   source name:cardiac ventricles|tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment: |geo loc name:missing|collection date:missing ventricle myd88 / untouched 1 Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q15 in a window of 5 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 99 with STAR 2.7.3a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 2.21.7 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. The raw count matrix was normalized with DESeq2 version 1.26.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Contrasts were created with DESeq2 based on the raw count matrix. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Gene counts were established with featureCounts 1.6.5 by aggregating reads overlapping exons excluding those overlapping multiple genes Liao et al. featureCounts: an efficient general purpose program for assigning sequence reads to genomic features. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: DanRer11 Supplementary files format and content: library normilzed counts cardiac ventricles untouched ventricles or cardiac cryoinjury at 1 or 24 hours prior to heart extraction RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture’s protocol Vazyme.   tissue:cardiac ventricles|cell type:ventricular cells|genotype:myd88 / |treatment: GSM8159060 GSM8159060: ventricle myd88 / untouched 1; Danio rerio; RNA Seq GSM8159060 r1 GSM8159060 1 RNA was isolated from 3 pooled ventricles or 3 pooled injured tissues per sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. 400ng of total RNA was used as input for VAHTS Stranded mRNA seq Library preparation V6 following manufacture's protocol Vazyme.   RNA-Seq TRANSCRIPTOMIC cDNA SINGLE ILLUMINA NextSeq 2000   SRP497025   loader:fastq load.py Pinelopi_Homo1_0h_pci_R1.fastq.gz fastq 2321007700.0 31228476.0 GSM8159060 r1 0:74.32 A:623574024;C:490503071;G:538918126;T:667825381;N:187098 74       623574024 490503071 538918126 667825381 187098 SRX24015858 SRS20810987 SRA1830778 MPI for heart and lung research MPI for heart and lung research                       B   usable mapping rate illumina nextseq_v2 unknown cdna_unspecified unknown bulk bulk bulk   Germany 2024-03-21 Undetermined Undetermined Heart Cardiovascular System
32476 32476 SRR29270149 SRX24787634 SRS21505104 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Mut 20 1   strain:AB|age:20|collection date:2023 06 10|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Mut 20 1 E10 E10 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Mut-20-1_S162_R1.fastq.gz foxl2l_Mut-20-1_S162_R2.fastq.gz fastq fastq 8940963680.0 29605840.0 foxl2l Mut 20 1 S162 R1.fastq.gz 0:151 1:151 A:2232167098;C:2229744850;G:2271326718;T:2207692629;N:32385 151 151     2232167098 2229744850 2271326718 2207692629 32385 SRX24787634 SRS21505104 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32477 32477 SRR29270150 SRX24787633 SRS21505103 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Het 20 3   strain:AB|age:20|collection date:2023 06 09|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Het 20 3 E9 E9 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Het-20-3_S161_R1.fastq.gz foxl2l_Het-20-3_S161_R2.fastq.gz fastq fastq 7038409282.0 23305991.0 foxl2l Het 20 3 S161 R1.fastq.gz 0:151 1:151 A:1766863186;C:1740008639;G:1787471686;T:1744039429;N:26342 151 151     1766863186 1740008639 1787471686 1744039429 26342 SRX24787633 SRS21505103 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32478 32478 SRR29270151 SRX24787632 SRS21505102 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Het 20 2   strain:AB|age:20|collection date:2023 06 08|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Het 20 2 E8 E8 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Het-20-2_S160_R1.fastq.gz foxl2l_Het-20-2_S160_R2.fastq.gz fastq fastq 6772505832.0 22425516.0 foxl2l Het 20 2 S160 R1.fastq.gz 0:151 1:151 A:1704124986;C:1673138074;G:1713003931;T:1682214009;N:24832 151 151     1704124986 1673138074 1713003931 1682214009 24832 SRX24787632 SRS21505102 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32479 32479 SRR29270152 SRX24787631 SRS21505101 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Het 20 1   strain:AB|age:20|collection date:2023 06 07|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Het 20 1 E7 E7 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Het-20-1_S159_R1.fastq.gz foxl2l_Het-20-1_S159_R2.fastq.gz fastq fastq 11685740812.0 38694506.0 foxl2l Het 20 1 S159 R1.fastq.gz 0:151 1:151 A:2939618668;C:2888861085;G:2958173208;T:2899044704;N:43147 151 151     2939618668 2888861085 2958173208 2899044704 43147 SRX24787631 SRS21505101 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32480 32480 SRR29270153 SRX24787630 SRS21505100 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Mut 15 3   strain:AB|age:15|collection date:2023 06 06|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Mut 15 3 E6 E6 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Mut-15-3_S158_R1.fastq.gz foxl2l_Mut-15-3_S158_R2.fastq.gz fastq fastq 9503789604.0 31469502.0 foxl2l Mut 15 3 S158 R1.fastq.gz 0:151 1:151 A:2393052443;C:2340958111;G:2411502428;T:2358240313;N:36309 151 151     2393052443 2340958111 2411502428 2358240313 36309 SRX24787630 SRS21505100 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32481 32481 SRR29270154 SRX24787629 SRS21505099 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Mut 15 2   strain:AB|age:15|collection date:2023 06 05|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Mut 15 2 E5 E5 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Mut-15-2_S157_R1.fastq.gz foxl2l_Mut-15-2_S157_R2.fastq.gz fastq fastq 7416837026.0 24559063.0 foxl2l Mut 15 2 S157 R1.fastq.gz 0:151 1:151 A:1865711045;C:1830489703;G:1881612508;T:1838995980;N:27790 151 151     1865711045 1830489703 1881612508 1838995980 27790 SRX24787629 SRS21505099 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32482 32482 SRR29270155 SRX24787628 SRS21505098 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Mut 15 1   strain:AB|age:15|collection date:2023 06 04|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Mut 15 1 E4 E4 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Mut-15-1_S156_R1.fastq.gz foxl2l_Mut-15-1_S156_R2.fastq.gz fastq fastq 7092721868.0 23485834.0 foxl2l Mut 15 1 S156 R1.fastq.gz 0:151 1:151 A:1764166761;C:1770534219;G:1820397492;T:1737597123;N:26273 151 151     1764166761 1770534219 1820397492 1737597123 26273 SRX24787628 SRS21505098 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32483 32483 SRR29270156 SRX24787627 SRS21505097 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Het 15 3   strain:AB|age:15|collection date:2023 06 03|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Het 15 3 E3 E3 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Het-15-3_S155_R1.fastq.gz foxl2l_Het-15-3_S155_R2.fastq.gz fastq fastq 8083606820.0 26766910.0 foxl2l Het 15 3 S155 R1.fastq.gz 0:151 1:151 A:2028557443;C:2001113164;G:2050610840;T:2003295953;N:29420 151 151     2028557443 2001113164 2050610840 2003295953 29420 SRX24787627 SRS21505097 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32484 32484 SRR29270157 SRX24787626 SRS21505096 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Mut 20 3   strain:AB|age:20|collection date:2023 06 12|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Mut 20 3 E12 E12 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Mut-20-3_S164_R1.fastq.gz foxl2l_Mut-20-3_S164_R2.fastq.gz fastq fastq 7474861796.0 24751198.0 foxl2l Mut 20 3 S164 R1.fastq.gz 0:151 1:151 A:1878881650;C:1849512621;G:1891142525;T:1855296720;N:28280 151 151     1878881650 1849512621 1891142525 1855296720 28280 SRX24787626 SRS21505096 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32485 32485 SRR29270158 SRX24787625 SRS21505095 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Mut 20 2   strain:AB|age:20|collection date:2023 06 11|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Mut 20 2 E11 E11 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Mut-20-2_S163_R1.fastq.gz foxl2l_Mut-20-2_S163_R2.fastq.gz fastq fastq 8203704066.0 27164583.0 foxl2l Mut 20 2 S163 R1.fastq.gz 0:151 1:151 A:2061693689;C:2030126562;G:2072980952;T:2038873198;N:29665 151 151     2061693689 2030126562 2072980952 2038873198 29665 SRX24787625 SRS21505095 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32486 32486 SRR29270159 SRX24787624 SRS21505094 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Het 15 2   strain:AB|age:15|collection date:2023 06 02|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Het 15 2 E2 E2 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Het-15-2_S154_R1.fastq.gz foxl2l_Het-15-2_S154_R2.fastq.gz fastq fastq 7868286860.0 26053930.0 foxl2l Het 15 2 S154 R1.fastq.gz 0:151 1:151 A:1972210357;C:1946891859;G:2008091153;T:1941064817;N:28674 151 151     1972210357 1946891859 2008091153 1941064817 28674 SRX24787624 SRS21505094 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32487 32487 SRR29270160 SRX24787623 SRS21505093 SRP511487 PRJNA1119569 RNA seq of zebrafish foxl2l mutant PRJNA1119569 Other Bulk seq of zebrafish foxl2l mutant at 15 dpf and 20 dpf. Each time point contain 3 heterozygous and 3 homozygous.         foxl2l Het 15 1   strain:AB|age:15|collection date:2023 06 01|geo loc name:China|sex:hermaphrodite|tissue:gonad|BioSampleModel:Model organism or animal                 foxl2l Het 15 1 E1 E1 50 ng of RNA was used to prepare VAHTS RNA seq Library using Universal V6 RNA seq Library Prep Kit for Illumina Vazeme NR604 01     RNA-Seq TRANSCRIPTOMIC PCR PAIRED ILLUMINA NextSeq 500   SRP511487     foxl2l_Het-15-1_S153_R1.fastq.gz foxl2l_Het-15-1_S153_R2.fastq.gz fastq fastq 7117391946.0 23567523.0 foxl2l Het 15 1 S153 R1.fastq.gz 0:151 1:151 A:1795668098;C:1752824783;G:1793720116;T:1775153584;N:25365 151 151     1795668098 1752824783 1793720116 1775153584 25365 SRX24787623 SRS21505093 SRA1887976 Institute of Hydrobiology, Chinese Academy of Sciences|Center for Fish Biology and Fishery Biotechnology Institute of Hydrobiology, Chinese Academy of Sciences                       B B biological fallback assumption illumina nextseq unknown random_priming unknown bulk bulk bulk   China 2024-06-03 Undetermined Undetermined Gonad Reproductive System
32850 32850 SRR29482329 SRX24993379 SRS21694843 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       MM rep5 [RNA Seq] GSM8340235   source name:mucosal melanoma|tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1|geo loc name:missing|collection date:missing MM rep5 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma mucosal melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1 GSM8340235 GSM8340235: MM rep5 [RNA Seq]; Danio rerio; RNA Seq GSM8340235 r1 GSM8340235 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI-Dr-F381.R2.fastq.gz MI-Dr-F381.R1.fastq.gz fastq fastq 12158543700.0 40528479.0 GSM8340235 r1 0:150 1:150 A:3249684583;C:2829283376;G:2878779006;T:3198464780;N:2331955 150 150     3249684583 2829283376 2878779006 3198464780 2331955 SRX24993379 SRS21694843 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.91528 0.91522 0.06081 0.06071 0.71662 0.72606 0.50019 0.49902 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32851 32851 SRR29482330 SRX24993378 SRS21694842 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       MM rep4 [RNA Seq] GSM8340234   source name:mucosal melanoma|tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1|geo loc name:missing|collection date:missing MM rep4 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma mucosal melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1 GSM8340234 GSM8340234: MM rep4 [RNA Seq]; Danio rerio; RNA Seq GSM8340234 r1 GSM8340234 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI-Dr-F380.R2.fastq.gz MI-Dr-F380.R1.fastq.gz fastq fastq 15136959300.0 50456531.0 GSM8340234 r1 0:150 1:150 A:3999982463;C:3565423997;G:3623206178;T:3945454250;N:2892412 150 150     3999982463 3565423997 3623206178 3945454250 2892412 SRX24993378 SRS21694842 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.91544 0.91681 0.05707 0.05629 0.71873 0.7278 0.50536 0.50794 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32852 32852 SRR29482331 SRX24993377 SRS21694841 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       MM rep3 [RNA Seq] GSM8340233   source name:mucosal melanoma|tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1|geo loc name:missing|collection date:missing MM rep3 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma mucosal melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1 GSM8340233 GSM8340233: MM rep3 [RNA Seq]; Danio rerio; RNA Seq GSM8340233 r1 GSM8340233 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI-Dr-F379.R1.fastq.gz MI-Dr-F379.R2.fastq.gz fastq fastq 19584405300.0 65281351.0 GSM8340233 r1 0:150 1:150 A:5193657176;C:4586793253;G:4681119346;T:5119062192;N:3773333 150 150     5193657176 4586793253 4681119346 5119062192 3773333 SRX24993377 SRS21694841 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.91009 0.91075 0.05605 0.05603 0.70709 0.71553 0.48633 0.5046 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32853 32853 SRR29482332 SRX24993376 SRS21694840 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       MM rep2 [RNA Seq] GSM8340232   source name:mucosal melanoma|tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1|geo loc name:missing|collection date:missing MM rep2 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma mucosal melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1 GSM8340232 GSM8340232: MM rep2 [RNA Seq]; Danio rerio; RNA Seq GSM8340232 r1 GSM8340232 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI-Dr-F378.R2.fastq.gz MI-Dr-F378.R1.fastq.gz fastq fastq 12509804100.0 41699347.0 GSM8340232 r1 0:150 1:150 A:3348127771;C:2902757443;G:2952121486;T:3304405412;N:2391988 150 150     3348127771 2902757443 2952121486 3304405412 2391988 SRX24993376 SRS21694840 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.90209 0.903 0.07387 0.07393 0.7232 0.73083 0.51976 0.52071 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32854 32854 SRR29482333 SRX24993375 SRS21694839 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       MM rep1 [RNA Seq] GSM8340231   source name:mucosal melanoma|tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1|geo loc name:missing|collection date:missing MM rep1 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma mucosal melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:mucosal melanoma|cell type:melanoma|genotype:roy / ; mitfa / fish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1 GSM8340231 GSM8340231: MM rep1 [RNA Seq]; Danio rerio; RNA Seq GSM8340231 r1 GSM8340231 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI-Dr-F377.R2.fastq.gz MI-Dr-F377.R1.fastq.gz fastq fastq 10304309400.0 34347698.0 GSM8340231 r1 0:150 1:150 A:2725877839;C:2430296510;G:2469399791;T:2676748684;N:1986576 150 150     2725877839 2430296510 2469399791 2676748684 1986576 SRX24993375 SRS21694839 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.9288 0.9297 0.05311 0.05279 0.7708 0.77918 0.53907 0.53683 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32855 32855 SRR29482334 SRX24993374 SRS21694838 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       CM rep3 [RNA Seq] GSM8340230   source name:cutaneous melanoma|tissue:cutaneous melanoma|cell type:melanoma|genotype:mitfa / ; tp53 / ; BRAFV600E fish injected with MCR:EGFP|geo loc name:missing|collection date:missing CM rep3 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma cutaneous melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:cutaneous melanoma|cell type:melanoma|genotype:mitfa / ; tp53 / ; BRAFV600E fish injected with MCR:EGFP GSM8340230 GSM8340230: CM rep3 [RNA Seq]; Danio rerio; RNA Seq GSM8340230 r1 GSM8340230 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI_12_USPD16098384-12_H2553BBXX_L8_2.fq.gz MI_12_USPD16098384-12_H2553BBXX_L8_1.fq.gz fastq fastq 10930590300.0 36435301.0 GSM8340230 r1 0:150 1:150 A:2979658653;C:2484668914;G:2536584911;T:2928246610;N:1431212 150 150     2979658653 2484668914 2536584911 2928246610 1431212 SRX24993374 SRS21694838 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.92203 0.92273 0.08582 0.08561 0.73815 0.73868 0.54966 0.54645 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32856 32856 SRR29482335 SRX24993373 SRS21694837 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       CM rep2 [RNA Seq] GSM8340229   source name:cutaneous melanoma|tissue:cutaneous melanoma|cell type:melanoma|genotype:mitfa / ; tp53 / ; BRAFV600E fish injected with MCR:EGFP|geo loc name:missing|collection date:missing CM rep2 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma cutaneous melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:cutaneous melanoma|cell type:melanoma|genotype:mitfa / ; tp53 / ; BRAFV600E fish injected with MCR:EGFP GSM8340229 GSM8340229: CM rep2 [RNA Seq]; Danio rerio; RNA Seq GSM8340229 r1 GSM8340229 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI_11_USPD16098384-11_H2553BBXX_L8_2.fq.gz MI_11_USPD16098384-11_H2553BBXX_L8_1.fq.gz fastq fastq 10972223700.0 36574079.0 GSM8340229 r1 0:150 1:150 A:2948309811;C:2536000818;G:2588828858;T:2897662110;N:1422103 150 150     2948309811 2536000818 2588828858 2897662110 1422103 SRX24993373 SRS21694837 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.92722 0.92814 0.06917 0.06867 0.71382 0.71575 0.5158 0.51662 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
32857 32857 SRR29482336 SRX24993372 SRS21694836 SRP515141 PRJNA1126244 Specific oncogene activation of the cell of origin in mucosal melanoma [RNA Seq] GSE270354 Transcriptome Analysis Mucosal melanoma MM is a deadly cancer derived from mucosal melanocytes. To test the consequences of MM genetics we develop a zebrafish model in which all melanocytes experience CCND1 expression and loss of PTEN and TP53. Surprisingly melanoma only develops from melanocytes lining internal organs analogous to the location of patient MM. We find that zebrafish MMs have a unique chromatin landscape from cutaneous melanoma. Internal melanocytes are labeled using a MM specific transcriptional enhancer. Normal zebrafish internal melanocytes share a gene expression signature with MMs. Patient and zebrafish MMs show increased migratory neural crest gene and decreased antigen presentation gene expression consistent with the increased metastatic behavior and decreased immunotherapy sensitivity of MM. Our work suggests the cell state of the originating melanocyte influences the behavior of derived melanomas. Our animal model phenotypically and transcriptionally mimics patient tumors allowing this model to be used for MM therapeutic discovery. As this is a non MAPK driven genetically engineered model of melanoma our work also has implications for the 15% of cutaneous melanoma patients who lack MAPK driving mutations. Overall design: Bulk RNA sequencing data from mucosal melanoma and cutaneous melanoma zebrafish models       CM rep1 [RNA Seq] GSM8340228   source name:cutaneous melanoma|tissue:cutaneous melanoma|cell type:melanoma|genotype:mitfa / ; tp53 / ; BRAFV600E fish injected with MCR:EGFP|geo loc name:missing|collection date:missing CM rep1 [RNA Seq] Cutadpt was used to remove adaptor sequences and low quality regions. The high quality reads were aligned to UCSC build danRer11 of zebrafish genome using Tophat 2.0.11 without xxx splicing form calls. Transcript abundance and differential expression were calculated with Cufflinks 2.2.1. Assembly: danRer11 Supplementary files format and content: .txt file contains differential gene expression of mucosal melanoma samples vs. cutaneous melanoma cutaneous melanoma   Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530 Melanomas generated from mitfa / ; tp53 / ; BRAFV600E zebrafish injected with MCR:EGFP or roy / ; mitfa / zebrafish injected with CRISPR MCR:tp53 sgRNA; CRISPR MCR:ptena/b sgRNA; MCR:CCND1were isolated for RNA seq. tissue:cutaneous melanoma|cell type:melanoma|genotype:mitfa / ; tp53 / ; BRAFV600E fish injected with MCR:EGFP GSM8340228 GSM8340228: CM rep1 [RNA Seq]; Danio rerio; RNA Seq GSM8340228 r1 GSM8340228 1 Tissue was disrupted using QIAshredder columns Qiagen 79656. DNA was removed and RNA was purified using columns Qiagen 74134. RNA was polyA selected NEB E7490. NEBNext Ultra RNA Library Prep Kit for Illumina NEB E7530   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP515141     MI_10_USPD16098384-10_H2553BBXX_L8_1.fq.gz MI_10_USPD16098384-10_H2553BBXX_L8_2.fq.gz fastq fastq 11662049100.0 38873497.0 GSM8340228 r1 0:150 1:150 A:3125745391;C:2697305234;G:2752722644;T:3084760577;N:1515254 150 150     3125745391 2697305234 2752722644 3084760577 1515254 SRX24993372 SRS21694836 SRA1904140 Insco Lab, Medical Oncology, Dana Farber Cancer Institute Insco Lab, Medical Oncology, Dana Farber Cancer Institute 2 0.92667 0.92674 0.0665 0.06609 0.7207 0.72107 0.52399 0.5179 150 150 B B biological fallback assumption illumina novaseq_era unknown poly_a nebnext bulk bulk bulk   United States 2024-06-20 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
33158 33158 SRR29791088 SRX25290435 SRS21969151 SRP519440 PRJNA1134759 Developmental trajectory and evolutionary origin of thymic mimetic cells [dataset 2] GSE272064 Transcriptome Analysis The generation of self tolerant repertoires of T cells depends on the expression of peripheral self antigens in the thymic epithelium and the presence of small populations of cells mimicking the diverse phenotypes of peripheral tissues. Whereas the molecular underpinnings of self antigen expression have been extensively studied the developmental origins and differentiation pathways of thymic mimetic cells remain to be identified. Moreover the histological identification of myoid and other peripheral cell types as components of the thymic microenvironment of many vertebrate species raises questions as to the evolutionary origin of this unique tolerance mechanism. Here we show that during mouse development mimetic cells appear in the microenvironment in two successive waves. Cells exhibiting transcriptional signatures characteristic of muscle ionocyte goblet and ciliated cells emerge before birth whereas others for instance those mimicking enterohepatic cells and skin keratinocytes appear postnatally. These two groups also respond differently to modulations of TEC progenitor pools caused by deletions of Foxn1 and Ascl1 expression of a hypomorphic Foxn1 transcription factor and overexpression of Bmp4 and Fgf7 signalling molecules. Differences in mimetic cell populations were also observed in thymic microenvironments reconstructed by replacement of mouse Foxn1 with evolutionarily ancient Foxn1/4 gene family members including the Foxn4 gene of the cephalochordate amphioxus and the Foxn4 and Foxn1 genes of a cartilaginous fish. Whereas some cell types such as ciliated cells develop in the thymus in the absence of Foxn1 mimetic cells appearing postnatally such as enterohepatic cells require the activity of the vertebrate specific transcription factor Foxn1. The thymus of cartilaginous fishes and the thymoid of lampreys a representative of jawless vertebrates that exhibit an alternative adaptive immune system also harbour cells expressing genes encoding peripheral tissue components such as the liver …       Dr thymus foxn1 / rep3 GSM8392364   source name:thymus|tissue:thymus|cell type:thymus cells|genotype:foxn1 / |geo loc name:missing|collection date:missing Dr thymus foxn1 / rep3 Transcriptomes were analyzed on the Galaxy platform. Adapters were trimmed with TrimGalore! version 0.4.3.1. Reads were aligned to the reference genome with Hisat2 version 2.1.0. Counts were generated with featureCounts version 1.6.1.0. Assembly: GRCz11 Supplementary files format and content: Tab delimited text files containing raw counts for each sample thymus   Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   tissue:thymus|cell type:thymus cells|genotype:foxn1 / GSM8392364 GSM8392364: Dr thymus foxn1 / rep3; Danio rerio; RNA Seq GSM8392364 r1 GSM8392364 1 Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP519440     BK6_R1.fastq.gz BK6_R2.fastq.gz fastq fastq 40416715568.0 133830184.0 GSM8392364 r1 0:151 1:151 A:11536946706;C:8490306261;G:9295609599;T:11092005423;N:1847579 151 151     11536946706 8490306261 9295609599 11092005423 1847579 SRX25290435 SRS21969151 SRA1922343 Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics 2 0.89276 0.89283 0.11419 0.11482 0.73306 0.73409 0.46305 0.46571 151 151 B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified nebnext bulk bulk bulk   Germany 2024-07-11 Undetermined Undetermined Thymus Hematopoietic System
33159 33159 SRR29791089 SRX25290434 SRS21969152 SRP519440 PRJNA1134759 Developmental trajectory and evolutionary origin of thymic mimetic cells [dataset 2] GSE272064 Transcriptome Analysis The generation of self tolerant repertoires of T cells depends on the expression of peripheral self antigens in the thymic epithelium and the presence of small populations of cells mimicking the diverse phenotypes of peripheral tissues. Whereas the molecular underpinnings of self antigen expression have been extensively studied the developmental origins and differentiation pathways of thymic mimetic cells remain to be identified. Moreover the histological identification of myoid and other peripheral cell types as components of the thymic microenvironment of many vertebrate species raises questions as to the evolutionary origin of this unique tolerance mechanism. Here we show that during mouse development mimetic cells appear in the microenvironment in two successive waves. Cells exhibiting transcriptional signatures characteristic of muscle ionocyte goblet and ciliated cells emerge before birth whereas others for instance those mimicking enterohepatic cells and skin keratinocytes appear postnatally. These two groups also respond differently to modulations of TEC progenitor pools caused by deletions of Foxn1 and Ascl1 expression of a hypomorphic Foxn1 transcription factor and overexpression of Bmp4 and Fgf7 signalling molecules. Differences in mimetic cell populations were also observed in thymic microenvironments reconstructed by replacement of mouse Foxn1 with evolutionarily ancient Foxn1/4 gene family members including the Foxn4 gene of the cephalochordate amphioxus and the Foxn4 and Foxn1 genes of a cartilaginous fish. Whereas some cell types such as ciliated cells develop in the thymus in the absence of Foxn1 mimetic cells appearing postnatally such as enterohepatic cells require the activity of the vertebrate specific transcription factor Foxn1. The thymus of cartilaginous fishes and the thymoid of lampreys a representative of jawless vertebrates that exhibit an alternative adaptive immune system also harbour cells expressing genes encoding peripheral tissue components such as the liver …       Dr thymus foxn1 / rep2 GSM8392363   source name:thymus|tissue:thymus|cell type:thymus cells|genotype:foxn1 / |geo loc name:missing|collection date:missing Dr thymus foxn1 / rep2 Transcriptomes were analyzed on the Galaxy platform. Adapters were trimmed with TrimGalore! version 0.4.3.1. Reads were aligned to the reference genome with Hisat2 version 2.1.0. Counts were generated with featureCounts version 1.6.1.0. Assembly: GRCz11 Supplementary files format and content: Tab delimited text files containing raw counts for each sample thymus   Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   tissue:thymus|cell type:thymus cells|genotype:foxn1 / GSM8392363 GSM8392363: Dr thymus foxn1 / rep2; Danio rerio; RNA Seq GSM8392363 r1 GSM8392363 1 Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP519440     BK5_R1.fastq.gz BK5_R2.fastq.gz fastq fastq 41734368446.0 138193273.0 GSM8392363 r1 0:151 1:151 A:12015023285;C:8850050726;G:9485443497;T:11381944831;N:1906107 151 151     12015023285 8850050726 9485443497 11381944831 1906107 SRX25290434 SRS21969152 SRA1922343 Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics 2 0.88856 0.88918 0.11978 0.11946 0.73003 0.732 0.44244 0.43125 151 151 B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified nebnext bulk bulk bulk   Germany 2024-07-11 Undetermined Undetermined Thymus Hematopoietic System
33160 33160 SRR29791090 SRX25290433 SRS21969150 SRP519440 PRJNA1134759 Developmental trajectory and evolutionary origin of thymic mimetic cells [dataset 2] GSE272064 Transcriptome Analysis The generation of self tolerant repertoires of T cells depends on the expression of peripheral self antigens in the thymic epithelium and the presence of small populations of cells mimicking the diverse phenotypes of peripheral tissues. Whereas the molecular underpinnings of self antigen expression have been extensively studied the developmental origins and differentiation pathways of thymic mimetic cells remain to be identified. Moreover the histological identification of myoid and other peripheral cell types as components of the thymic microenvironment of many vertebrate species raises questions as to the evolutionary origin of this unique tolerance mechanism. Here we show that during mouse development mimetic cells appear in the microenvironment in two successive waves. Cells exhibiting transcriptional signatures characteristic of muscle ionocyte goblet and ciliated cells emerge before birth whereas others for instance those mimicking enterohepatic cells and skin keratinocytes appear postnatally. These two groups also respond differently to modulations of TEC progenitor pools caused by deletions of Foxn1 and Ascl1 expression of a hypomorphic Foxn1 transcription factor and overexpression of Bmp4 and Fgf7 signalling molecules. Differences in mimetic cell populations were also observed in thymic microenvironments reconstructed by replacement of mouse Foxn1 with evolutionarily ancient Foxn1/4 gene family members including the Foxn4 gene of the cephalochordate amphioxus and the Foxn4 and Foxn1 genes of a cartilaginous fish. Whereas some cell types such as ciliated cells develop in the thymus in the absence of Foxn1 mimetic cells appearing postnatally such as enterohepatic cells require the activity of the vertebrate specific transcription factor Foxn1. The thymus of cartilaginous fishes and the thymoid of lampreys a representative of jawless vertebrates that exhibit an alternative adaptive immune system also harbour cells expressing genes encoding peripheral tissue components such as the liver …       Dr thymus foxn1 / rep1 GSM8392362   source name:thymus|tissue:thymus|cell type:thymus cells|genotype:foxn1 / |geo loc name:missing|collection date:missing Dr thymus foxn1 / rep1 Transcriptomes were analyzed on the Galaxy platform. Adapters were trimmed with TrimGalore! version 0.4.3.1. Reads were aligned to the reference genome with Hisat2 version 2.1.0. Counts were generated with featureCounts version 1.6.1.0. Assembly: GRCz11 Supplementary files format and content: Tab delimited text files containing raw counts for each sample thymus   Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   tissue:thymus|cell type:thymus cells|genotype:foxn1 / GSM8392362 GSM8392362: Dr thymus foxn1 / rep1; Danio rerio; RNA Seq GSM8392362 r1 GSM8392362 1 Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP519440     BK4_R2.fastq.gz BK4_R1.fastq.gz fastq fastq 39302001858.0 130139079.0 GSM8392362 r1 0:151 1:151 A:11220466966;C:8305776940;G:9105878447;T:10668104948;N:1774557 151 151     11220466966 8305776940 9105878447 10668104948 1774557 SRX25290433 SRS21969150 SRA1922343 Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics 2 0.89299 0.89318 0.11306 0.1139 0.74123 0.74345 0.45102 0.46093 151 151 B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified nebnext bulk bulk bulk   Germany 2024-07-11 Undetermined Undetermined Thymus Hematopoietic System
33161 33161 SRR29791091 SRX25290432 SRS21969149 SRP519440 PRJNA1134759 Developmental trajectory and evolutionary origin of thymic mimetic cells [dataset 2] GSE272064 Transcriptome Analysis The generation of self tolerant repertoires of T cells depends on the expression of peripheral self antigens in the thymic epithelium and the presence of small populations of cells mimicking the diverse phenotypes of peripheral tissues. Whereas the molecular underpinnings of self antigen expression have been extensively studied the developmental origins and differentiation pathways of thymic mimetic cells remain to be identified. Moreover the histological identification of myoid and other peripheral cell types as components of the thymic microenvironment of many vertebrate species raises questions as to the evolutionary origin of this unique tolerance mechanism. Here we show that during mouse development mimetic cells appear in the microenvironment in two successive waves. Cells exhibiting transcriptional signatures characteristic of muscle ionocyte goblet and ciliated cells emerge before birth whereas others for instance those mimicking enterohepatic cells and skin keratinocytes appear postnatally. These two groups also respond differently to modulations of TEC progenitor pools caused by deletions of Foxn1 and Ascl1 expression of a hypomorphic Foxn1 transcription factor and overexpression of Bmp4 and Fgf7 signalling molecules. Differences in mimetic cell populations were also observed in thymic microenvironments reconstructed by replacement of mouse Foxn1 with evolutionarily ancient Foxn1/4 gene family members including the Foxn4 gene of the cephalochordate amphioxus and the Foxn4 and Foxn1 genes of a cartilaginous fish. Whereas some cell types such as ciliated cells develop in the thymus in the absence of Foxn1 mimetic cells appearing postnatally such as enterohepatic cells require the activity of the vertebrate specific transcription factor Foxn1. The thymus of cartilaginous fishes and the thymoid of lampreys a representative of jawless vertebrates that exhibit an alternative adaptive immune system also harbour cells expressing genes encoding peripheral tissue components such as the liver …       Dr thymus foxn1+/+ rep3 GSM8392361   source name:thymus|tissue:thymus|cell type:thymus cells|genotype:foxn1+/+|geo loc name:missing|collection date:missing Dr thymus foxn1+/+ rep3 Transcriptomes were analyzed on the Galaxy platform. Adapters were trimmed with TrimGalore! version 0.4.3.1. Reads were aligned to the reference genome with Hisat2 version 2.1.0. Counts were generated with featureCounts version 1.6.1.0. Assembly: GRCz11 Supplementary files format and content: Tab delimited text files containing raw counts for each sample thymus   Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   tissue:thymus|cell type:thymus cells|genotype:foxn1+/+ GSM8392361 GSM8392361: Dr thymus foxn1+/+ rep3; Danio rerio; RNA Seq GSM8392361 r1 GSM8392361 1 Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP519440     BK3_R1.fastq.gz BK3_R2.fastq.gz fastq fastq 37243022634.0 123321267.0 GSM8392361 r1 0:151 1:151 A:10858514997;C:7805630226;G:8359994769;T:10217208022;N:1674620 151 151     10858514997 7805630226 8359994769 10217208022 1674620 SRX25290432 SRS21969149 SRA1922343 Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics 2 0.87732 0.87686 0.20353 0.20336 0.73261 0.7343 0.49192 0.4924 151 151 B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified nebnext bulk bulk bulk   Germany 2024-07-11 Undetermined Undetermined Thymus Hematopoietic System
33162 33162 SRR29791092 SRX25290431 SRS21969148 SRP519440 PRJNA1134759 Developmental trajectory and evolutionary origin of thymic mimetic cells [dataset 2] GSE272064 Transcriptome Analysis The generation of self tolerant repertoires of T cells depends on the expression of peripheral self antigens in the thymic epithelium and the presence of small populations of cells mimicking the diverse phenotypes of peripheral tissues. Whereas the molecular underpinnings of self antigen expression have been extensively studied the developmental origins and differentiation pathways of thymic mimetic cells remain to be identified. Moreover the histological identification of myoid and other peripheral cell types as components of the thymic microenvironment of many vertebrate species raises questions as to the evolutionary origin of this unique tolerance mechanism. Here we show that during mouse development mimetic cells appear in the microenvironment in two successive waves. Cells exhibiting transcriptional signatures characteristic of muscle ionocyte goblet and ciliated cells emerge before birth whereas others for instance those mimicking enterohepatic cells and skin keratinocytes appear postnatally. These two groups also respond differently to modulations of TEC progenitor pools caused by deletions of Foxn1 and Ascl1 expression of a hypomorphic Foxn1 transcription factor and overexpression of Bmp4 and Fgf7 signalling molecules. Differences in mimetic cell populations were also observed in thymic microenvironments reconstructed by replacement of mouse Foxn1 with evolutionarily ancient Foxn1/4 gene family members including the Foxn4 gene of the cephalochordate amphioxus and the Foxn4 and Foxn1 genes of a cartilaginous fish. Whereas some cell types such as ciliated cells develop in the thymus in the absence of Foxn1 mimetic cells appearing postnatally such as enterohepatic cells require the activity of the vertebrate specific transcription factor Foxn1. The thymus of cartilaginous fishes and the thymoid of lampreys a representative of jawless vertebrates that exhibit an alternative adaptive immune system also harbour cells expressing genes encoding peripheral tissue components such as the liver …       Dr thymus foxn1+/+ rep2 GSM8392360   source name:thymus|tissue:thymus|cell type:thymus cells|genotype:foxn1+/+|geo loc name:missing|collection date:missing Dr thymus foxn1+/+ rep2 Transcriptomes were analyzed on the Galaxy platform. Adapters were trimmed with TrimGalore! version 0.4.3.1. Reads were aligned to the reference genome with Hisat2 version 2.1.0. Counts were generated with featureCounts version 1.6.1.0. Assembly: GRCz11 Supplementary files format and content: Tab delimited text files containing raw counts for each sample thymus   Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   tissue:thymus|cell type:thymus cells|genotype:foxn1+/+ GSM8392360 GSM8392360: Dr thymus foxn1+/+ rep2; Danio rerio; RNA Seq GSM8392360 r1 GSM8392360 1 Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP519440     BK2_R1.fastq.gz BK2_R2.fastq.gz fastq fastq 34154139756.0 113093178.0 GSM8392360 r1 0:151 1:151 A:9754575779;C:7198913431;G:7834944597;T:9364172876;N:1533073 151 151     9754575779 7198913431 7834944597 9364172876 1533073 SRX25290431 SRS21969148 SRA1922343 Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics 2 0.87955 0.88145 0.18817 0.18856 0.72707 0.72839 0.49921 0.49737 151 151 B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified nebnext bulk bulk bulk   Germany 2024-07-11 Undetermined Undetermined Thymus Hematopoietic System
33163 33163 SRR29791093 SRX25290430 SRS21969147 SRP519440 PRJNA1134759 Developmental trajectory and evolutionary origin of thymic mimetic cells [dataset 2] GSE272064 Transcriptome Analysis The generation of self tolerant repertoires of T cells depends on the expression of peripheral self antigens in the thymic epithelium and the presence of small populations of cells mimicking the diverse phenotypes of peripheral tissues. Whereas the molecular underpinnings of self antigen expression have been extensively studied the developmental origins and differentiation pathways of thymic mimetic cells remain to be identified. Moreover the histological identification of myoid and other peripheral cell types as components of the thymic microenvironment of many vertebrate species raises questions as to the evolutionary origin of this unique tolerance mechanism. Here we show that during mouse development mimetic cells appear in the microenvironment in two successive waves. Cells exhibiting transcriptional signatures characteristic of muscle ionocyte goblet and ciliated cells emerge before birth whereas others for instance those mimicking enterohepatic cells and skin keratinocytes appear postnatally. These two groups also respond differently to modulations of TEC progenitor pools caused by deletions of Foxn1 and Ascl1 expression of a hypomorphic Foxn1 transcription factor and overexpression of Bmp4 and Fgf7 signalling molecules. Differences in mimetic cell populations were also observed in thymic microenvironments reconstructed by replacement of mouse Foxn1 with evolutionarily ancient Foxn1/4 gene family members including the Foxn4 gene of the cephalochordate amphioxus and the Foxn4 and Foxn1 genes of a cartilaginous fish. Whereas some cell types such as ciliated cells develop in the thymus in the absence of Foxn1 mimetic cells appearing postnatally such as enterohepatic cells require the activity of the vertebrate specific transcription factor Foxn1. The thymus of cartilaginous fishes and the thymoid of lampreys a representative of jawless vertebrates that exhibit an alternative adaptive immune system also harbour cells expressing genes encoding peripheral tissue components such as the liver …       Dr thymus foxn1+/+ rep1 GSM8392359   source name:thymus|tissue:thymus|cell type:thymus cells|genotype:foxn1+/+|geo loc name:missing|collection date:missing Dr thymus foxn1+/+ rep1 Transcriptomes were analyzed on the Galaxy platform. Adapters were trimmed with TrimGalore! version 0.4.3.1. Reads were aligned to the reference genome with Hisat2 version 2.1.0. Counts were generated with featureCounts version 1.6.1.0. Assembly: GRCz11 Supplementary files format and content: Tab delimited text files containing raw counts for each sample thymus   Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   tissue:thymus|cell type:thymus cells|genotype:foxn1+/+ GSM8392359 GSM8392359: Dr thymus foxn1+/+ rep1; Danio rerio; RNA Seq GSM8392359 r1 GSM8392359 1 Thymus tissue was explanted and placed into TRI reagent Sigma Aldrich. RNA was extracted following standard protocols. Each library consists of a pool of RNA from 3 animals. Libraries were constructed with the NEBNext Low Input RNA Library Preparation kit. Library preparation was carried out by the Deep Sequencing core facility at the Max Planck Institute for Immunobiology and Epigenetics according to their standard protocols.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq 6000   SRP519440     BK1_R2.fastq.gz BK1_R1.fastq.gz fastq fastq 48045652026.0 159091563.0 GSM8392359 r1 0:151 1:151 A:13986882382;C:9969611893;G:10712447624;T:13374538759;N:2171368 151 151     13986882382 9969611893 10712447624 13374538759 2171368 SRX25290430 SRS21969147 SRA1922343 Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics Boehm, Developmental Immunology, Max Planck Institute for Immunobiology and Epigenetics 2 0.87379 0.87656 0.21786 0.2191 0.73815 0.73975 0.49869 0.49808 151 151 B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified nebnext bulk bulk bulk   Germany 2024-07-11 Undetermined Undetermined Thymus Hematopoietic System
33706 33706 SRR30621736 SRX26043972 SRS22614948 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 21 dpi sample 2 GSM8506783   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 21 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506783 GSM8506783: wild type 21 dpi sample 2; Danio rerio; RNA Seq GSM8506783 r1 GSM8506783 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_21dpi_2_1.fq.gz wt_21dpi_2_2.fq.gz fastq fastq 7641378600.0 25471262.0 GSM8506783 r1 0:150 1:150 A:2079206538;C:1754420100;G:1752583773;T:2055108610;N:59579 150 150     2079206538 1754420100 1752583773 2055108610 59579 SRX26043972 SRS22614948 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33707 33707 SRR30621737 SRX26043971 SRS22614947 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 21 dpi sample 1 GSM8506782   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 21 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506782 GSM8506782: wild type 21 dpi sample 1; Danio rerio; RNA Seq GSM8506782 r1 GSM8506782 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_21dpi_1_1.fq.gz wt_21dpi_1_2.fq.gz fastq fastq 8663480400.0 28878268.0 GSM8506782 r1 0:150 1:150 A:2358947065;C:1986782909;G:1985349061;T:2332333991;N:67374 150 150     2358947065 1986782909 1985349061 2332333991 67374 SRX26043971 SRS22614947 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33708 33708 SRR30621738 SRX26043970 SRS22614946 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 7 dpi sample 2 GSM8506781   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 7 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506781 GSM8506781: wild type 7 dpi sample 2; Danio rerio; RNA Seq GSM8506781 r1 GSM8506781 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_7dpi_2_1.fq.gz wt_7dpi_2_2.fq.gz fastq fastq 8414243254.0 28200981.0 GSM8506781 r1 0:149.18 1:149.19 A:2273220495;C:1952762066;G:1928310101;T:2259829448;N:121144 149 149     2273220495 1952762066 1928310101 2259829448 121144 SRX26043970 SRS22614946 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33709 33709 SRR30621739 SRX26043969 SRS22614945 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 7 dpi sample 1 GSM8506780   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 7 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506780 GSM8506780: wild type 7 dpi sample 1; Danio rerio; RNA Seq GSM8506780 r1 GSM8506780 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_7dpi_1_1.fq.gz wt_7dpi_1_2.fq.gz fastq fastq 6047075346.0 20278990.0 GSM8506780 r1 0:149.09 1:149.10 A:1633289750;C:1403959505;G:1385683308;T:1624058844;N:83939 149 149     1633289750 1403959505 1385683308 1624058844 83939 SRX26043969 SRS22614945 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33710 33710 SRR30621740 SRX26043968 SRS22614944 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 2 dpi sample 2 GSM8506779   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 2 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506779 GSM8506779: wild type 2 dpi sample 2; Danio rerio; RNA Seq GSM8506779 r1 GSM8506779 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_2dpi_2_1.fq.gz wt_2dpi_2_2.fq.gz fastq fastq 6501507640.0 21847961.0 GSM8506779 r1 0:148.79 1:148.79 A:1751063874;C:1515880337;G:1494689364;T:1739782712;N:91353 148 148     1751063874 1515880337 1494689364 1739782712 91353 SRX26043968 SRS22614944 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33711 33711 SRR30621741 SRX26043967 SRS22614943 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 2 dpi sample 1 GSM8506778   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 2 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506778 GSM8506778: wild type 2 dpi sample 1; Danio rerio; RNA Seq GSM8506778 r1 GSM8506778 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_2dpi_1_1.fq.gz wt_2dpi_1_2.fq.gz fastq fastq 6367687936.0 21382594.0 GSM8506778 r1 0:148.89 1:148.90 A:1717644272;C:1482451492;G:1461128189;T:1706373727;N:90256 148 148     1717644272 1482451492 1461128189 1706373727 90256 SRX26043967 SRS22614943 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33712 33712 SRR30621742 SRX26043966 SRS22614942 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 0 dpi sample 2 GSM8506777   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 0 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506777 GSM8506777: wild type 0 dpi sample 2; Danio rerio; RNA Seq GSM8506777 r1 GSM8506777 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_0dpi_2_1.fq.gz wt_0dpi_2_2.fq.gz fastq fastq 10558249200.0 35194164.0 GSM8506777 r1 0:150 1:150 A:2893792627;C:2407838089;G:2396125046;T:2860411622;N:81816 150 150     2893792627 2407838089 2396125046 2860411622 81816 SRX26043966 SRS22614942 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33713 33713 SRR30621743 SRX26043965 SRS22614941 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       wild type 0 dpi sample 1 GSM8506776   source name:Heart ventricle|tissue:Heart ventricle|genotype:wild type|geo loc name:missing|collection date:missing wild type 0 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:wild type GSM8506776 GSM8506776: wild type 0 dpi sample 1; Danio rerio; RNA Seq GSM8506776 r1 GSM8506776 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     wt_0dpi_1_1.fq.gz wt_0dpi_1_2.fq.gz fastq fastq 10931466600.0 36438222.0 GSM8506776 r1 0:150 1:150 A:2980386716;C:2504687323;G:2500279931;T:2946028049;N:84581 150 150     2980386716 2504687323 2500279931 2946028049 84581 SRX26043965 SRS22614941 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33714 33714 SRR30621744 SRX26043964 SRS22614940 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 21 dpi sample 2 GSM8506775   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 21 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506775 GSM8506775: nr4a1 mutant 21 dpi sample 2; Danio rerio; RNA Seq GSM8506775 r1 GSM8506775 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_21_2_1.fq.gz nr4a1_21_2_2.fq.gz fastq fastq 8089743600.0 26965812.0 GSM8506775 r1 0:150 1:150 A:2204157080;C:1856260728;G:1849823127;T:2179439591;N:63074 150 150     2204157080 1856260728 1849823127 2179439591 63074 SRX26043964 SRS22614940 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33715 33715 SRR30621745 SRX26043963 SRS22614939 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 21 dpi sample 1 GSM8506774   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 21 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506774 GSM8506774: nr4a1 mutant 21 dpi sample 1; Danio rerio; RNA Seq GSM8506774 r1 GSM8506774 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_21_1_1.fq.gz nr4a1_21_1_2.fq.gz fastq fastq 8268177900.0 27560593.0 GSM8506774 r1 0:150 1:150 A:2258410899;C:1890202189;G:1886482508;T:2233018477;N:63827 150 150     2258410899 1890202189 1886482508 2233018477 63827 SRX26043963 SRS22614939 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33716 33716 SRR30621746 SRX26043962 SRS22614938 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 7 dpi sample 2 GSM8506773   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 7 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506773 GSM8506773: nr4a1 mutant 7 dpi sample 2; Danio rerio; RNA Seq GSM8506773 r1 GSM8506773 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_7dpi_2_1.fq.gz nr4a1_7dpi_2_2.fq.gz fastq fastq 5512600871.0 18517476.0 GSM8506773 r1 0:148.84 1:148.85 A:1483061100;C:1285068800;G:1269689220;T:1474711048;N:70703 148 148     1483061100 1285068800 1269689220 1474711048 70703 SRX26043962 SRS22614938 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33717 33717 SRR30621747 SRX26043961 SRS22614937 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 7 dpi sample 1 GSM8506772   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 7 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506772 GSM8506772: nr4a1 mutant 7 dpi sample 1; Danio rerio; RNA Seq GSM8506772 r1 GSM8506772 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_7dpi_1_1.fq.gz nr4a1_7dpi_1_2.fq.gz fastq fastq 6780831475.0 22750295.0 GSM8506772 r1 0:149.03 1:149.03 A:1831140932;C:1575183518;G:1554676178;T:1819734347;N:96500 149 149     1831140932 1575183518 1554676178 1819734347 96500 SRX26043961 SRS22614937 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33718 33718 SRR30621748 SRX26043960 SRS22614936 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 2 dpi sample 2 GSM8506771   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 2 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506771 GSM8506771: nr4a1 mutant 2 dpi sample 2; Danio rerio; RNA Seq GSM8506771 r1 GSM8506771 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_2dpi_2_1.fq.gz nr4a1_2dpi_2_2.fq.gz fastq fastq 6503531797.0 21834092.0 GSM8506771 r1 0:148.93 1:148.93 A:1739648368;C:1527224071;G:1508002505;T:1728567175;N:89678 148 148     1739648368 1527224071 1508002505 1728567175 89678 SRX26043960 SRS22614936 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33719 33719 SRR30621749 SRX26043959 SRS22614935 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 2 dpi sample 1 GSM8506770   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 2 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506770 GSM8506770: nr4a1 mutant 2 dpi sample 1; Danio rerio; RNA Seq GSM8506770 r1 GSM8506770 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_2dpi_1_1.fq.gz nr4a1_2dpi_1_2.fq.gz fastq fastq 5645476838.0 18937309.0 GSM8506770 r1 0:149.05 1:149.06 A:1522889953;C:1312356884;G:1296118643;T:1514035483;N:75875 149 149     1522889953 1312356884 1296118643 1514035483 75875 SRX26043959 SRS22614935 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33720 33720 SRR30621750 SRX26043958 SRS22614934 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 0 dpi sample 2 GSM8506769   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 0 dpi sample 2 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506769 GSM8506769: nr4a1 mutant 0 dpi sample 2; Danio rerio; RNA Seq GSM8506769 r1 GSM8506769 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_0dpi_2_1.fq.gz nr4a1_0dpi_2_2.fq.gz fastq fastq 9184630800.0 30615436.0 GSM8506769 r1 0:150 1:150 A:2514442400;C:2095585016;G:2092520078;T:2482011445;N:71861 150 150     2514442400 2095585016 2092520078 2482011445 71861 SRX26043958 SRS22614934 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33721 33721 SRR30621751 SRX26043957 SRS22614933 SRP531880 PRJNA1159283 Nr4a1 Modulates Inflammation and Heart Regeneration in Zebrafish GSE276850 Transcriptome Analysis Recent findings have highlighted the complex role of inflammation in zebrafish heart regeneration demonstrating that while inflammation is essential for initiating transient fibrosis and tissue repair chronic inflammation and unresolved fibrosis could impede full regenerative recovery. In this study we identified the nuclear receptor Nr4a1 as a critical regulator of this regenerative process in zebrafish. Loss of Nr4a1 function led to a prolonged and excessive inflammatory response disrupted neutrophil migration delayed fibrin clearance and ultimately impaired heart regeneration. Transcriptome wide RNA seq analysis at different injury stages revealed molecular disruptions associated with dysregulated inflammation and fibrosis in Nr4a1 mutants. Notably partial inhibition of the pro inflammatory cytokine Tnf a rescued heart regeneration in the nr4a1 mutants highlighting the therapeutic potential of modulating inflammation. Our findings suggest that Nr4a1 plays a crucial role in orchestrating the immune response during heart regeneration and may serve as a valuable target for enhancing cardiac repair following injury. Overall design: To elucidate the molecular basis of the phenotypes observed in the nr4a1 mutant we performed transcriptome wide bulk RNA sequencing on the ventricles from both control and mutant hearts at several key time points. Baseline transcriptomic profiles were established from uninjured hearts to compare the cardiac transcriptomics of the wildtype control and nr4a1 mutant. Given the critical involvement of inflammation in heart regeneration samples were also collected at 2 and 7 dpci corresponding to stages marked by an active inflammatory response. Moreover to elucidate the prolonged fibrosis phenotype in the late injury stage we performed transcriptomic analysis on hearts collected at 21 dpci.       nr4a1 mutant 0 dpi sample 1 GSM8506768   source name:Heart ventricle|tissue:Heart ventricle|genotype:nr4a1 mutant|geo loc name:missing|collection date:missing nr4a1 mutant 0 dpi sample 1 RNA seq raw data quality was checked by FastQC https://www.bioinformatics.babraham.ac.uk/projects/fastqc/. RNA seq were aligned to the zebrafish reference genome using STARDobin et al. 2013. Gene expression was quantified as gene hit counts reads per gene using FeatureCountsLiao et al. 2014. Assembly: Danio rerio zebrafish genome assembly GRCz11 danRer11 Supplementary files format and content: txt data file include raw counts for each sample Heart ventricle   Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   tissue:Heart ventricle|genotype:nr4a1 mutant GSM8506768 GSM8506768: nr4a1 mutant 0 dpi sample 1; Danio rerio; RNA Seq GSM8506768 r1 GSM8506768 1 Total RNA was isolated from zebrafish ventricles using Trizol Invitrogen. Reverse transcription was performed using SuperScript IV VILO Master Mix Invitrogen. For RNA seq library preparation and Illumina RNA seq were performed by Novogene.   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina NovaSeq X Plus   SRP531880     nr4a1_0dpi_1_1.fq.gz nr4a1_0dpi_1_2.fq.gz fastq fastq 9290140800.0 30967136.0 GSM8506768 r1 0:150 1:150 A:2540516970;C:2120755706;G:2115163242;T:2513633143;N:71739 150 150     2540516970 2120755706 2115163242 2513633143 71739 SRX26043957 SRS22614933 SRA1968119 The University of North Carolina The University of North Carolina                       B B biological fallback assumption illumina novaseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2024-09-10 Undetermined Undetermined Heart Cardiovascular System
33894 33894 SRR30866028 SRX26263941 SRS22803195 SRP536275 PRJNA1168148 Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq] GSE278653 Transcriptome Analysis Dysregulated melanocyte state transitions are a pivotal driver of melanoma development highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b a glycosyl transferase involved in selective N glycan branching enriched in pigment progenitors as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell McSC pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb Kit and Tyrp1 to be under the control of Mgat4b. Additionally mislocalization of Gamma catenin Jup explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N glycan branching in both melanocyte development and melanoma initiation suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…       m4b mut melanoma biol rep 2 GSM8552314   source name:skin|tissue:skin|cell type:melanoma|genotype:mgat4b mutant|treatment:MAZERATI|geo loc name:missing|collection date:missing m4b mut melanoma biol rep 2 Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample skin   The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   tissue:skin|cell type:melanoma|genotype:mgat4b mutant|treatment:MAZERATI GSM8552314 GSM8552314: m4b mut melanoma biol rep 2; Danio rerio; RNA Seq GSM8552314 r1 GSM8552314 1 The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA NextSeq 2000   SRP536275     MKO2_S39_R1_001.fastq.gz MKO2_S39_R2_001.fastq.gz fastq fastq 3705364625.0 14164066.0 GSM8552314 r1 0:126.72 1:134.89 A:785806700;C:949078797;G:1178279032;T:784972987;N:7227109 126 134     785806700 949078797 1178279032 784972987 7227109 SRX26263941 SRS22803195 SRA1984938 Pigment Cell Biology Lab, CSIR-IGIB Pigment Cell Biology Lab, CSIR-IGIB                       B B biological fallback assumption illumina nextseq_v2 unknown cdna_unspecified trueseq sc_generic bulk bulk   India 2024-10-02 Undetermined Undetermined Skin Surface Structure
33895 33895 SRR30866029 SRX26263940 SRS22803194 SRP536275 PRJNA1168148 Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq] GSE278653 Transcriptome Analysis Dysregulated melanocyte state transitions are a pivotal driver of melanoma development highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b a glycosyl transferase involved in selective N glycan branching enriched in pigment progenitors as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell McSC pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb Kit and Tyrp1 to be under the control of Mgat4b. Additionally mislocalization of Gamma catenin Jup explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N glycan branching in both melanocyte development and melanoma initiation suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…       m4b mut melanoma biol rep 1 GSM8552313   source name:skin|tissue:skin|cell type:melanoma|genotype:mgat4b mutant|treatment:MAZERATI|geo loc name:missing|collection date:missing m4b mut melanoma biol rep 1 Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample skin   The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   tissue:skin|cell type:melanoma|genotype:mgat4b mutant|treatment:MAZERATI GSM8552313 GSM8552313: m4b mut melanoma biol rep 1; Danio rerio; RNA Seq GSM8552313 r1 GSM8552313 1 The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA NextSeq 2000   SRP536275     MKO1_S38_R1_001.fastq.gz MKO1_S38_R2_001.fastq.gz fastq fastq 4779377372.0 18058294.0 GSM8552313 r1 0:128.72 1:135.94 A:1016908920;C:1236613888;G:1502465334;T:1018053808;N:5335422 128 135     1016908920 1236613888 1502465334 1018053808 5335422 SRX26263940 SRS22803194 SRA1984938 Pigment Cell Biology Lab, CSIR-IGIB Pigment Cell Biology Lab, CSIR-IGIB                       B B biological fallback assumption illumina nextseq_v2 unknown cdna_unspecified trueseq sc_generic bulk bulk   India 2024-10-02 Undetermined Undetermined Skin Surface Structure
33896 33896 SRR30866030 SRX26263939 SRS22803193 SRP536275 PRJNA1168148 Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq] GSE278653 Transcriptome Analysis Dysregulated melanocyte state transitions are a pivotal driver of melanoma development highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b a glycosyl transferase involved in selective N glycan branching enriched in pigment progenitors as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell McSC pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb Kit and Tyrp1 to be under the control of Mgat4b. Additionally mislocalization of Gamma catenin Jup explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N glycan branching in both melanocyte development and melanoma initiation suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…       wild type melanoma control biol rep 2 GSM8552312   source name:skin|tissue:skin|cell type:melanoma|genotype:WT|treatment:MAZERATI|geo loc name:missing|collection date:missing wild type melanoma control biol rep 2 Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample skin   The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   tissue:skin|cell type:melanoma|genotype:WT|treatment:MAZERATI GSM8552312 GSM8552312: wild type melanoma control biol rep 2; Danio rerio; RNA Seq GSM8552312 r1 GSM8552312 1 The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA NextSeq 2000   SRP536275     EV2_S37_R1_001.fastq.gz EV2_S37_R2_001.fastq.gz fastq fastq 5427379509.0 19981504.0 GSM8552312 r1 0:133.16 1:138.46 A:1136639418;C:1414638483;G:1736492639;T:1137614638;N:1994331 133 138     1136639418 1414638483 1736492639 1137614638 1994331 SRX26263939 SRS22803193 SRA1984938 Pigment Cell Biology Lab, CSIR-IGIB Pigment Cell Biology Lab, CSIR-IGIB                       B B biological fallback assumption illumina nextseq_v2 unknown cdna_unspecified trueseq sc_generic bulk bulk   India 2024-10-02 Undetermined Undetermined Skin Surface Structure
33897 33897 SRR30866031 SRX26263938 SRS22803192 SRP536275 PRJNA1168148 Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq] GSE278653 Transcriptome Analysis Dysregulated melanocyte state transitions are a pivotal driver of melanoma development highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b a glycosyl transferase involved in selective N glycan branching enriched in pigment progenitors as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell McSC pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb Kit and Tyrp1 to be under the control of Mgat4b. Additionally mislocalization of Gamma catenin Jup explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N glycan branching in both melanocyte development and melanoma initiation suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…       wild type melanoma control biol rep 1 GSM8552311   source name:skin|tissue:skin|cell type:melanoma|genotype:WT|treatment:MAZERATI|geo loc name:missing|collection date:missing wild type melanoma control biol rep 1 Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample skin   The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   tissue:skin|cell type:melanoma|genotype:WT|treatment:MAZERATI GSM8552311 GSM8552311: wild type melanoma control biol rep 1; Danio rerio; RNA Seq GSM8552311 r1 GSM8552311 1 The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA NextSeq 2000   SRP536275     EV1_S36_R1_001.fastq.gz EV1_S36_R2_001.fastq.gz fastq fastq 5248108957.0 19087024.0 GSM8552311 r1 0:135.12 1:139.84 A:1112163842;C:1354895660;G:1658732932;T:1120342985;N:1973538 135 139     1112163842 1354895660 1658732932 1120342985 1973538 SRX26263938 SRS22803192 SRA1984938 Pigment Cell Biology Lab, CSIR-IGIB Pigment Cell Biology Lab, CSIR-IGIB                       B B biological fallback assumption illumina nextseq_v2 unknown cdna_unspecified trueseq sc_generic bulk bulk   India 2024-10-02 Undetermined Undetermined Skin Surface Structure
33898 33898 SRR30866032 SRX26263937 SRS22803191 SRP536275 PRJNA1168148 Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq] GSE278653 Transcriptome Analysis Dysregulated melanocyte state transitions are a pivotal driver of melanoma development highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b a glycosyl transferase involved in selective N glycan branching enriched in pigment progenitors as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell McSC pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb Kit and Tyrp1 to be under the control of Mgat4b. Additionally mislocalization of Gamma catenin Jup explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N glycan branching in both melanocyte development and melanoma initiation suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…       melanophore biol rep 2 GSM8552310   source name:skin|tissue:skin|cell type:melanophore|genotype:WT|treatment:No|geo loc name:missing|collection date:missing melanophore biol rep 2 Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample skin   The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   tissue:skin|cell type:melanophore|genotype:WT|treatment:No GSM8552310 GSM8552310: melanophore biol rep 2; Danio rerio; RNA Seq GSM8552310 r1 GSM8552310 1 The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA NextSeq 2000   SRP536275     WT2_S41_R1_001.fastq.gz WT2_S41_R2_001.fastq.gz fastq fastq 4636631881.0 16340506.0 GSM8552310 r1 0:140.47 1:143.28 A:1114533149;C:1104066636;G:1293649625;T:1122672029;N:1710442 140 143     1114533149 1104066636 1293649625 1122672029 1710442 SRX26263937 SRS22803191 SRA1984938 Pigment Cell Biology Lab, CSIR-IGIB Pigment Cell Biology Lab, CSIR-IGIB                       B B biological fallback assumption illumina nextseq_v2 unknown cdna_unspecified trueseq sc_generic bulk bulk   India 2024-10-02 Undetermined Undetermined Skin Surface Structure
33899 33899 SRR30866033 SRX26263936 SRS22803190 SRP536275 PRJNA1168148 Mgat4b mediated selective N glycosyl modification regulates melanocyte development and melanoma progression [bulk RNA seq] GSE278653 Transcriptome Analysis Dysregulated melanocyte state transitions are a pivotal driver of melanoma development highlighting the need to identify key regulators of these processes. Understanding these factors is key to know how normal melanocyte functions and shift towards initiation of melanoma. Our study identifies Mgat4b a glycosyl transferase involved in selective N glycan branching enriched in pigment progenitors as a key regulator of directional melanocyte migration and establishment of Melanocyte stem cell McSC pool during early development in zebrafish and mammalian melanocytes. Single cell RNA sequencing analysis in zebrafish upon targeted disruption of Mgat4b reveals that a subset of melanocytes marked by aberrant galectin expression are impaired in migration and are lost. Lectin binding proteomic analysis reveals the glycosylation of key melanocyte proteins Gpnmb Kit and Tyrp1 to be under the control of Mgat4b. Additionally mislocalization of Gamma catenin Jup explains the observed defects in cell adhesion and migration to be regulated by mgat4b but not its isozyme mgat4a. Our meta analysis further revealed that melanoma patients with both the BrafV600E mutation and elevated Mgat4b levels have significantly worse survival outcomes compared to those with only the BrafV600E mutation. By leveraging the MAZERATI platform to model BrafV600E driver mutation in vivo we show that Mgat4b mutant cells fail to aggregate and initiate tumors. Our study underscores the importance of selective N glycan branching in both melanocyte development and melanoma initiation suggesting a Mitf controlled Mgat4b as a promising therapeutic target for melanoma treatment. Overall design: To investigate the mechanisms that inhibit mutant cells from initiating melanoma in the absence of mgat4b we utilized mature melanophores and melanoma cells from the skin of five zebrafish including both MAZERATI wild type and MAZERATI zebrafish carrying mgat4b mutations. We then performed gene expression profiling analysis using data obtained from RNA seq of m…       melanophore biol rep 1 GSM8552309   source name:skin|tissue:skin|cell type:melanophore|genotype:WT|treatment:No|geo loc name:missing|collection date:missing melanophore biol rep 1 Raw fastq files were trimmed using trimmomatic to remove adaptors and retain high quality reads. The reads were then aligned with zebrafish reference assembly GRCz11 using STAR. Featurecounts was used to calculate raw counts from the aligned reads. Assembly: GRCz11 Supplementary files format and content: tab delimited text file including raw counts for each sample skin   The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   tissue:skin|cell type:melanophore|genotype:WT|treatment:No GSM8552309 GSM8552309: melanophore biol rep 1; Danio rerio; RNA Seq GSM8552309 r1 GSM8552309 1 The cell isolation process involved density gradient centrifugation followed by RNA extraction using Trizol method. Illumina standard total RNA prep kit was used for library construction   RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA NextSeq 2000   SRP536275     WT1_S40_R1_001.fastq.gz WT1_S40_R2_001.fastq.gz fastq fastq 5185761246.0 18118534.0 GSM8552309 r1 0:141.81 1:144.40 A:1231235669;C:1235759770;G:1476864583;T:1240636871;N:1264353 141 144     1231235669 1235759770 1476864583 1240636871 1264353 SRX26263936 SRS22803190 SRA1984938 Pigment Cell Biology Lab, CSIR-IGIB Pigment Cell Biology Lab, CSIR-IGIB                       B B biological fallback assumption illumina nextseq_v2 unknown cdna_unspecified trueseq sc_generic bulk bulk   India 2024-10-02 Undetermined Undetermined Skin Surface Structure
37134 37134 SRR997335 SRX355601 SRS483796 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Control rep4 GSM1234963   source name:Heart Control|tissue:heart Heart Control rep4 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Control   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234963 GSM1234963: Heart Control rep4; Danio rerio; RNA Seq GSM1234963   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234963 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     C3PO_0053_s_7_sequence.txt.gz fastq 1111882122.0 28509798.0 GSM1234963 r1 0:39 A:239964076;C:229590501;G:337557042;T:303257677;N:1512826 39       239964076 229590501 337557042 303257677 1512826 SRX355601 SRS483796 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.11195   0.03776   0.98871   0.16576   39   B   usable mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37135 37135 SRR997334 SRX355600 SRS483795 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Control rep3 GSM1234962   source name:Heart Control|tissue:heart Heart Control rep3 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Control   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234962 GSM1234962: Heart Control rep3; Danio rerio; RNA Seq GSM1234962   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234962 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     C3PO_0053_s_6_sequence.txt.gz fastq 1221305046.0 31315514.0 GSM1234962 r1 0:39 A:263520584;C:251263128;G:372262308;T:332218529;N:2040497 39       263520584 251263128 372262308 332218529 2040497 SRX355600 SRS483795 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.11552   0.03865   0.98679   0.1927   39   B   usable mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37136 37136 SRR997333 SRX355599 SRS483794 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Control rep2 GSM1234961   source name:Heart Control|tissue:heart Heart Control rep2 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Control   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234961 GSM1234961: Heart Control rep2; Danio rerio; RNA Seq GSM1234961   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234961 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     R2D2_0122_s_7_sequence.txt.gz fastq 1462542939.0 37501101.0 GSM1234961 r1 0:39 A:313173840;C:298865755;G:440814004;T:409066990;N:622350 39       313173840 298865755 440814004 409066990 622350 SRX355599 SRS483794 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.01745   0.00554   0.99101   0.42928   39   B   usable mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37137 37137 SRR997332 SRX355598 SRS483793 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Control rep1 GSM1234960   source name:Heart Control|tissue:heart Heart Control rep1 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Control   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234960 GSM1234960: Heart Control rep1; Danio rerio; RNA Seq GSM1234960   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234960 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     R2D2_0122_s_6_sequence.txt.gz fastq 1447346355.0 37111445.0 GSM1234960 r1 0:39 A:311132663;C:297266985;G:441400778;T:396960907;N:585022 39       311132663 297266985 441400778 396960907 585022 SRX355598 SRS483793 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.06118   0.01997   0.98752   0.43741   39   B   usable mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37138 37138 SRR997331 SRX355597 SRS483792 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Resected rep4 GSM1234959   source name:Heart Resected|tissue:heart Heart Resected rep4 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Resected   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234959 GSM1234959: Heart Resected rep4; Danio rerio; RNA Seq GSM1234959   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234959 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     C3PO_0053_s_5_sequence.txt.gz fastq 703519557.0 18038963.0 GSM1234959 r1 0:39 A:142685665;C:144259439;G:215526965;T:199924689;N:1122799 39       142685665 144259439 215526965 199924689 1122799 SRX355597 SRS483792 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.00172   0.00045   0.99738   0.34873   39   T   under 1.2% mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37139 37139 SRR997330 SRX355596 SRS483791 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Resected rep3 GSM1234958   source name:Heart Resected|tissue:heart Heart Resected rep3 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Resected   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234958 GSM1234958: Heart Resected rep3; Danio rerio; RNA Seq GSM1234958   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234958 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     C3PO_0053_s_4_sequence.txt.gz fastq 918978177.0 23563543.0 GSM1234958 r1 0:39 A:188056254;C:191217660;G:283318445;T:255042736;N:1343082 39       188056254 191217660 283318445 255042736 1343082 SRX355596 SRS483791 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.09453   0.03085   0.98559   0.18337   39   B   usable mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37140 37140 SRR997329 SRX355595 SRS483789 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Resected rep2 GSM1234957   source name:Heart Resected|tissue:heart Heart Resected rep2 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Resected   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234957 GSM1234957: Heart Resected rep2; Danio rerio; RNA Seq GSM1234957   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234957 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     R2D2_0122_s_5_sequence.txt.gz fastq 1420874247.0 36432673.0 GSM1234957 r1 0:39 A:290914118;C:295973738;G:440368910;T:393019696;N:597785 39       290914118 295973738 440368910 393019696 597785 SRX355595 SRS483789 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.00472   0.00131   0.99431   0.42832   39   T   under 1.2% mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
37141 37141 SRR997328 SRX355594 SRS483790 SRP030036 PRJNA219641 Comparative transcriptome profiling of the injured zebrafish and mouse hearts identifies miRNA dependent repair pathways GSE51018 Transcriptome Analysis The mammalian heart has poor regenerative capacity following injury. In contrast certain lower vertebrates such as zebrafish retain a robust capacity for regeneration into adult life. Here we use an integrated approach to identify evolutionary conserved regenerative miRNA dependant regulatory circuits in the heart. We identified novel miRNA dependant networks involved in critical biological pathways which are differentially utilized between the infarcted mouse heart and the regenerating zebrafish heart. Overall design: 2 conditions 4 biological replicates per condition parent bioproject:PRJNA219631 pubmed:26857418   Heart Resected rep1 GSM1234956   source name:Heart Resected|tissue:heart Heart Resected rep1 Base calling was with Illumina GAP Pipeline Software v1.70 Sequence reads were processed to remove the adaptor sequences and reformatted to FASTA files using the FASTX Toolkit Sequences were aligned to mouse mature microRNA sequences from miRBase Version 17 and non coding RNA sequences Rfam Version 10 using MEGABLAST with a word size of 8 nucleotides. The criteria for counting a sequence match were if the % query was >=90% of the target sequence and if there were <= 2 mismatches over the alignment. The % query was calculated as a/q x p where a= alignment length q= query length and p= percent identity over aligned region. The matches against miRBase were parsed and the top matches based on % query were selected. If a sequence had more than one top match against different database sequences it was excluded from the subsequent analysis. Matches to Rfam were only taken into account for sequences not matching miRBase. Genome build: miRBase17 Supplementary files format and content: Raw count data for microRNAs were normalized to the relative size of each library using R/Bioconductor package DESeq estimateSizeFactors function. Count data are provided in tab delimited format Heart Resected   Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001   tissue:heart GSM1234956 GSM1234956: Heart Resected rep1; Danio rerio; RNA Seq GSM1234956   1 Total RNA was isolated using Trizol Invitrogen. RNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 BioanalyzerRNA quantities and quality were assessed using a NanoDrop ND 1000 spectrophotometer or an Agilent 2100 Bioanalyzer. Libraries of small RNAs for sequencing were prepared using the DGE Small RNA Sample Kit Alternative v1.5 Protocol Illumina; San Diego California according to the protocol supplied with the reagents Protocol Rev. A published February 2009 and using 1ug of total RNA. One lane of each library was sequenced on the Genome Analyzer IIx Illumina using the 36 Cycle Sequencing Kit v5 and v4 flowcell and cluster reagents Catalog FC 104 5020 and GD 300 1001 GEO Accession:GSM1234956 RNA-Seq TRANSCRIPTOMIC size fractionation SINGLE ILLUMINA Illumina Genome Analyzer II   SRP030036     C3PO_0054_s_8_sequence.txt.gz fastq 1073339514.0 27521526.0 GSM1234956 r1 0:39 A:223670054;C:219603945;G:328718329;T:300891777;N:455409 39       223670054 219603945 328718329 300891777 455409 SRX355594 SRS483790 SRA101779 GEO Vital-IT, SIB Swiss Institute of Bioinformatics 1 0.05133   0.01643   0.9893   0.25792   39   B   usable mapping rate illumina early_illumina unknown size_fractionation unknown bulk bulk bulk   Switzerland 2013-09-19 Undetermined Undetermined Heart Cardiovascular System
45035 45035 SRR6494615 SRX3583941 SRS2852966 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   12.2B GSM2915057   tissue:Leukemia cells|replicate number:2|self renewal capacity:low|background strain:CG1|cell type:blood 12.2B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:low|background strain:CG1|cell type:blood GSM2915057 GSM2915057: 12.2B; Danio rerio; RNA Seq GSM2915057   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915057 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     12.2B_R1.fastq.gz 12.2B_R2.fastq.gz fastq fastq 4198177098.0 41158599.0 GSM2915057 r1 0:51 1:51 A:933297427;C:1160638498;G:1167269516;T:931714756;N:5256901 51 51     933297427 1160638498 1167269516 931714756 5256901 SRX3583941 SRS2852966 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.94442 0.95328 0.19284 0.1878 0.83668 0.83792 0.64423 0.61017 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45036 45036 SRR6494614 SRX3583940 SRS2852967 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   12.2A GSM2915056   tissue:Leukemia cells|replicate number:1|self renewal capacity:low|background strain:CG1|cell type:blood 12.2A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:low|background strain:CG1|cell type:blood GSM2915056 GSM2915056: 12.2A; Danio rerio; RNA Seq GSM2915056   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915056 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     12.2A_R1.fastq.gz 12.2A_R2.fastq.gz fastq fastq 4664784100.0 46647841.0 GSM2915056 r1 0:50 1:50 A:1104404665;C:1222868717;G:1231852847;T:1104961679;N:696192 50 50     1104404665 1222868717 1231852847 1104961679 696192 SRX3583940 SRS2852967 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.92243 0.93608 0.22772 0.22103 0.80411 0.80626 0.61604 0.59999 50 50 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45037 45037 SRR6494613 SRX3583939 SRS2852965 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   10.2B GSM2915055   tissue:Leukemia cells|replicate number:2|self renewal capacity:low|background strain:CG1|cell type:blood 10.2B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:low|background strain:CG1|cell type:blood GSM2915055 GSM2915055: 10.2B; Danio rerio; RNA Seq GSM2915055   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915055 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     10.2B_R1.fastq.gz 10.2B_R2.fastq.gz fastq fastq 4065465714.0 39857507.0 GSM2915055 r1 0:51 1:51 A:1004499069;C:1015058139;G:1027707268;T:1013076822;N:5124416 51 51     1004499069 1015058139 1027707268 1013076822 5124416 SRX3583939 SRS2852965 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.92877 0.93609 0.2145 0.21044 0.78879 0.79034 0.57017 0.5699 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45038 45038 SRR6494612 SRX3583938 SRS2852964 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   10.2A GSM2915054   tissue:Leukemia cells|replicate number:1|self renewal capacity:low|background strain:CG1|cell type:blood 10.2A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:low|background strain:CG1|cell type:blood GSM2915054 GSM2915054: 10.2A; Danio rerio; RNA Seq GSM2915054   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915054 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     10.2A_R1.fastq.gz 10.2A_R2.fastq.gz fastq fastq 5825997800.0 58259978.0 GSM2915054 r1 0:50 1:50 A:1452695020;C:1453278793;G:1458683037;T:1460466496;N:874454 50 50     1452695020 1453278793 1458683037 1460466496 874454 SRX3583938 SRS2852964 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.92886 0.9381 0.21573 0.21305 0.78632 0.78813 0.55808 0.56378 50 50 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45039 45039 SRR6494611 SRX3583937 SRS2852963 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   9.2B GSM2915053   tissue:Leukemia cells|replicate number:2|self renewal capacity:low|background strain:CG1|cell type:blood 9.2B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:low|background strain:CG1|cell type:blood GSM2915053 GSM2915053: 9.2B; Danio rerio; RNA Seq GSM2915053   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915053 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     9.2B_R1.fastq.gz 9.2B_R2.fastq.gz fastq fastq 4506740256.0 44183728.0 GSM2915053 r1 0:51 1:51 A:1112271704;C:1123458923;G:1145952359;T:1119515017;N:5542253 51 51     1112271704 1123458923 1145952359 1119515017 5542253 SRX3583937 SRS2852963 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.92746 0.93269 0.23417 0.23028 0.79904 0.8032 0.54807 0.56848 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45040 45040 SRR6494610 SRX3583936 SRS2852962 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   9.2A GSM2915052   tissue:Leukemia cells|replicate number:1|self renewal capacity:low|background strain:CG1|cell type:blood 9.2A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:low|background strain:CG1|cell type:blood GSM2915052 GSM2915052: 9.2A; Danio rerio; RNA Seq GSM2915052   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915052 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     9.2A_R1.fastq.gz 9.2A_R2.fastq.gz fastq fastq 4360921770.0 42754135.0 GSM2915052 r1 0:51 1:51 A:1079666608;C:1084041944;G:1104190687;T:1087055139;N:5967392 51 51     1079666608 1084041944 1104190687 1087055139 5967392 SRX3583936 SRS2852962 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.93401 0.93834 0.24172 0.23839 0.79543 0.79853 0.54668 0.56646 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45041 45041 SRR6494609 SRX3583935 SRS2852961 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   7.2.1B GSM2915051   tissue:Leukemia cells|replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood 7.2.1B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915051 GSM2915051: 7.2.1B; Danio rerio; RNA Seq GSM2915051   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915051 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     7.2.1B_R1.fastq.gz 7.2.1B_R2.fastq.gz fastq fastq 4269804864.0 41860832.0 GSM2915051 r1 0:51 1:51 A:1061177239;C:1059094144;G:1073327634;T:1070820946;N:5384901 51 51     1061177239 1059094144 1073327634 1070820946 5384901 SRX3583935 SRS2852961 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.93904 0.94983 0.27598 0.27453 0.80353 0.80732 0.56729 0.5674 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45042 45042 SRR6494608 SRX3583934 SRS2852960 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   7.2.1A GSM2915050   tissue:Leukemia cells|replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood 7.2.1A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915050 GSM2915050: 7.2.1A; Danio rerio; RNA Seq GSM2915050   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915050 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     7.2.1A_R1.fastq.gz 7.2.1A_R2.fastq.gz fastq fastq 4365552700.0 43655527.0 GSM2915050 r1 0:50 1:50 A:1081366107;C:1100458538;G:1102308246;T:1080751188;N:668621 50 50     1081366107 1100458538 1102308246 1080751188 668621 SRX3583934 SRS2852960 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.95152 0.95745 0.25194 0.2485 0.80436 0.80377 0.48817 0.50698 50 50 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45043 45043 SRR6494607 SRX3583933 SRS2852959 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   13.1.1B GSM2915049   tissue:Leukemia cells|replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood 13.1.1B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915049 GSM2915049: 13.1.1B; Danio rerio; RNA Seq GSM2915049   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915049 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     13.1.1B_R1.fastq.gz 13.1.1B_R2.fastq.gz fastq fastq 4354271166.0 42688933.0 GSM2915049 r1 0:51 1:51 A:1064019486;C:1100195568;G:1114361396;T:1070229465;N:5465251 51 51     1064019486 1100195568 1114361396 1070229465 5465251 SRX3583933 SRS2852959 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.93925 0.94875 0.25209 0.24836 0.80837 0.80996 0.47839 0.58777 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45044 45044 SRR6494606 SRX3583932 SRS2853049 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   13.1.1A GSM2915048   tissue:Leukemia cells|replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood 13.1.1A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915048 GSM2915048: 13.1.1A; Danio rerio; RNA Seq GSM2915048   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915048 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     13.1.1A_R1.fastq.gz 13.1.1A_R2.fastq.gz fastq fastq 4640640100.0 46406401.0 GSM2915048 r1 0:50 1:50 A:1200822095;C:1111931040;G:1117066830;T:1210105773;N:714362 50 50     1200822095 1111931040 1117066830 1210105773 714362 SRX3583932 SRS2853049 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.91613 0.92428 0.32822 0.32518 0.79101 0.79243 0.56679 0.56385 50 50 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45045 45045 SRR6494605 SRX3583931 SRS2852958 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   15.2B GSM2915047   tissue:Leukemia cells|replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood 15.2B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915047 GSM2915047: 15.2B; Danio rerio; RNA Seq GSM2915047   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915047 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     15.2B_R1.fastq.gz 15.2B_R2.fastq.gz fastq fastq 4734832758.0 46419929.0 GSM2915047 r1 0:51 1:51 A:1173476233;C:1180848673;G:1186821491;T:1187703528;N:5982833 51 51     1173476233 1180848673 1186821491 1187703528 5982833 SRX3583931 SRS2852958 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.93596 0.94402 0.29428 0.29343 0.81174 0.81292 0.59979 0.57701 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45046 45046 SRR6494604 SRX3583930 SRS2852957 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   15.2A GSM2915046   tissue:Leukemia cells|replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood 15.2A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915046 GSM2915046: 15.2A; Danio rerio; RNA Seq GSM2915046   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915046 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     15.2A_R1.fastq.gz 15.2A_R2.fastq.gz fastq fastq 4146122700.0 41461227.0 GSM2915046 r1 0:50 1:50 A:1018153184;C:1052958176;G:1054611038;T:1019770342;N:629960 50 50     1018153184 1052958176 1054611038 1019770342 629960 SRX3583930 SRS2852957 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.95101 0.95735 0.2546 0.25126 0.81497 0.81497 0.51581 0.58721 50 50 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45047 45047 SRR6494603 SRX3583929 SRS2852956 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   2.1B GSM2915045   tissue:Leukemia cells|replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood 2.1B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915045 GSM2915045: 2.1B; Danio rerio; RNA Seq GSM2915045   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915045 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     2.1B_R1.fastq.gz 2.1B_R2.fastq.gz fastq fastq 4485073008.0 43971304.0 GSM2915045 r1 0:51 1:51 A:1077166487;C:1155027635;G:1165169697;T:1082191047;N:5518142 51 51     1077166487 1155027635 1165169697 1082191047 5518142 SRX3583929 SRS2852956 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.94959 0.95559 0.25458 0.25289 0.8238 0.82475 0.55503 0.59704 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45048 45048 SRR6494602 SRX3583928 SRS2852955 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   2.1A GSM2915044   tissue:Leukemia cells|replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood 2.1A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915044 GSM2915044: 2.1A; Danio rerio; RNA Seq GSM2915044   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915044 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     2.1A_R1.fastq.gz 2.1A_R2.fastq.gz fastq fastq 4648689474.0 45575387.0 GSM2915044 r1 0:51 1:51 A:1150739906;C:1156762106;G:1174418869;T:1160455829;N:6312764 51 51     1150739906 1156762106 1174418869 1160455829 6312764 SRX3583928 SRS2852955 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.93443 0.9425 0.3037 0.30192 0.81675 0.82035 0.5641 0.55492 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45049 45049 SRR6494601 SRX3583927 SRS2852953 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   8.3B GSM2915043   tissue:Leukemia cells|replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood 8.3B Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:2|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915043 GSM2915043: 8.3B; Danio rerio; RNA Seq GSM2915043   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915043 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     8.3B_R1.fastq.gz 8.3B_R2.fastq.gz fastq fastq 4463531424.0 43760112.0 GSM2915043 r1 0:51 1:51 A:1113035544;C:1103847188;G:1123396000;T:1117789326;N:5463366 51 51     1113035544 1103847188 1123396000 1117789326 5463366 SRX3583927 SRS2852953 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.94125 0.95133 0.17024 0.16786 0.78924 0.79255 0.54779 0.54529 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor
45050 45050 SRR6494600 SRX3583926 SRS2852954 SRP130950 PRJNA428951 Cell of origin dictates aggression and stem cell activity in acute lymphoblastic leukemia GSE108855 Transcriptome Analysis Subclassification of lymphoid neoplasms is often based on the presumed cell of origin based on T and B progenitor gene expression and the effect of cell lineage on influencing functional characteristics such as aggression and self renewal capacity is largely unknown accounted for in part by lack of experimental models to address these questions. Here we have used transgenic zebrafish to create the first models of Myc induced B ALL and mixed phenotypic B/T ALL opening new avenues for studying the these leukemias in the zebrafish. Our work has utilized syngeneic strain zebrafish limiting dilution cell transplantation and the widely reported rag2 Myc transgenic model to provide new understanding of how strain differences can underlie leukemia onset in the zebrafish model. Even more importantly our work now for the first time has allowed assessment of cell lineage on dictating aggression and leukemia stem cell frequency independent of the underlying oncogenic driver. In total our work uncoveres that T ALLs are more aggressive and have higher numbers of leukemia stem cells when compared with B ALL and mixed phenotypic ALL. Furthermore analysis of our biphenotypic B/T ALL suggests that B cell pathways lock cells in less aggressive and lower stem cell fates and are dominant in regulating these processes when T cell pathways are co regulated within ALL cells. Overall design: The goal of our study is to determine the transcriptional profiles of high and low self renewing capacity tumors. 20 samples total: 11 unique samples 9 samples with biological replicates 6 high self renewing tumors >1% cells could initiate leukemia and 5 low self renewing tumors <1% of cells could initiate leukemia.   pubmed:29749398   8.3A GSM2915042   tissue:Leukemia cells|replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood 8.3A Demultiplexed reads were aligned using STARDobin et al. 2013 to GRCz10. We used picard to filter out PCR duplicates and also removed reads aligning to rRNA intervals. We then assigned counts to each gene using featureCountsLiao Y Smyth GK and Shi W 2014. Genome build: GRCz10 Supplementary files format and content: count matrix provided as supplementary file Leukemia cells   Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform.   replicate number:1|self renewal capacity:high|background strain:CG1|cell type:blood GSM2915042 GSM2915042: 8.3A; Danio rerio; RNA Seq GSM2915042   1 Leukemia cell pellets were mixed 350ul of QIAGEN RLT buffer containing 1% 2 mercaptoethanol followed by RNA isolation using the RNAeasy Mini kit QIAGEN. RNA samples were prepped and sequenced on the Illumina HiSeq 2000 platform as previously described in Tang et al. PMID 28878000. RNA from bulk tumors were reverse transcribed and sequenced on the Illumina HiSeq 2000 platform. GEO Accession:GSM2915042 RNA-Seq TRANSCRIPTOMIC cDNA PAIRED ILLUMINA Illumina HiSeq 2000   SRP130950     8.3A_R1.fastq.gz 8.3A_R2.fastq.gz fastq fastq 4393347876.0 43072038.0 GSM2915042 r1 0:51 1:51 A:1076247371;C:1106828053;G:1120376486;T:1083936462;N:5959504 51 51     1076247371 1106828053 1120376486 1083936462 5959504 SRX3583926 SRS2852954 SRA649887 GEO Pathology, Massachusetts General Hospital 2 0.94915 0.95442 0.17122 0.16696 0.79732 0.79744 0.56274 0.56769 51 51 B B biological fallback assumption illumina hiseq_era unknown cdna_unspecified unknown bulk bulk bulk   United States 2018-01-08 Undetermined Undetermined Cancer or Tumor Cancer or Tumor

Next page

Advanced export

JSON shape: default, array, newline-delimited

CSV options: 

CREATE TABLE run_metadata("run.accession" VARCHAR, "experiment.accession" VARCHAR, "sample.accession" VARCHAR, "study.accession" VARCHAR, bioproject VARCHAR, "study.title" VARCHAR, "study.alias" VARCHAR, "study.type" VARCHAR, "study.abstract" VARCHAR, "study.attributes" VARCHAR, "study.PMIDs" VARCHAR, "sample.description" VARCHAR, "sample.title" VARCHAR, "sample.alias" VARCHAR, "sample.centername" VARCHAR, "sample.attributes" VARCHAR, "GEOsample.title" VARCHAR, "GEOsample.dataprocessing" VARCHAR, "GEOsample.source" VARCHAR, "GEOsample.treatmentprotocol" VARCHAR, "GEOsample.extractprotocol" VARCHAR, "GEOsample.growthprotocol" VARCHAR, "GEOsample.characteristics" VARCHAR, "GEOsample.accession" VARCHAR, "experiment.title" VARCHAR, "experiment.alias" VARCHAR, "experiment.library_name" VARCHAR, "experiment.design_description" VARCHAR, "experiment.library_construction_protocol" VARCHAR, "experiment.attributes" VARCHAR, "experiment.library_strategy" VARCHAR, "experiment.library_source" VARCHAR, "experiment.library_selection" VARCHAR, "experiment.library_layout" VARCHAR, "experiment.platform" VARCHAR, "experiment.instrument_model" VARCHAR, "experiment.spot_descriptor" VARCHAR, "experiment.study_ref" VARCHAR, "run.title" VARCHAR, "run.attributes" VARCHAR, "run.filename" VARCHAR, "run.semantic_name" VARCHAR, "run.total_bases" DOUBLE, "run.total_spots" DOUBLE, "run.alias" VARCHAR, "run.read_lengths" VARCHAR, "run.base_counts" VARCHAR, "run.r1_length" BIGINT, "run.r2_length" BIGINT, "run.r3_length" BIGINT, "run.r4_length" BIGINT, "run.Acount" BIGINT, "run.Ccount" BIGINT, "run.Gcount" BIGINT, "run.Tcount" BIGINT, "run.Ncount" BIGINT, "run.experiment" VARCHAR, "run.pool_member" VARCHAR, "submission.accession" VARCHAR, "submission.srasource" VARCHAR, "submission.bioprojectsource" VARCHAR, "seqdetective.n_mates" BIGINT, "seqdetective.mapping_rate.mate1" DOUBLE, "seqdetective.mapping_rate.mate2" DOUBLE, "seqdetective.nofeature_rate.mate1" DOUBLE, "seqdetective.nofeature_rate.mate2" DOUBLE, "seqdetective.sparsity.mate1" DOUBLE, "seqdetective.sparsity.mate2" DOUBLE, "seqdetective.pos_strand_rate.mate1" DOUBLE, "seqdetective.pos_strand_rate.mate2" DOUBLE, "seqdetective.readlen.mate1" BIGINT, "seqdetective.readlen.mate2" BIGINT, "seqdetective.judgement.mate1" VARCHAR, "seqdetective.judgement.mate2" VARCHAR, "seqdetective.judgement.reason" VARCHAR, platform_family VARCHAR, instrument_generation VARCHAR, read_bias VARCHAR, selection_class VARCHAR, prep_kit VARCHAR, sc_or_bulk VARCHAR, tech_class VARCHAR, technology VARCHAR, tech_variant VARCHAR, "submission.bioprojectsource.country" VARCHAR, earliest_date DATE, devstage_curation VARCHAR, devstage_curation_coarse VARCHAR, tissue_curation VARCHAR, tissue_curation_coarse VARCHAR);;
CREATE INDEX idx_run_bioproject ON run_metadata(bioproject);;
CREATE INDEX idx_run_run_accession ON run_metadata("run.accession");;