{"database": "metadata", "table": "run_metadata", "is_view": false, "human_description_en": "where devstage_curation = \"Undetermined\" and tissue_curation = \"Heart\"", "rows": [[25320, "SRR25810878", "SRX21533024", "SRS18745490", "SRP457576", "PRJNA1010780", "Effect of egr3 knockout on gene expression of dissected zebrafish hearts", "GSE241935", "Transcriptome Analysis", "To screen for Egr3 targets mediating cardiac valve development we assessed gene expression on dissected hearts of egr3 mutants and wild type siblings. Overall design: To evaluate the transcriptional differences underlying the egr3 mutant phenotype we conducted a bulk RNA seq analysis in dissected zebrafish hearts at 48 hpf. We dissected 20 hearts for each biological duplicate of egr3 mutant and wild type sibling samples in cold DMEM with 10% FBS. Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u00b5l of RNase free water. Analysis of the obtained reads confirmed the 11bp deletion in the mutant samples. 1. Boezio G. L. M. et al. The developing epicardium regulates cardiac chamber morphogenesis by promoting cardiomyocyte growth. Dis Model Mech 16 2023. https://doi.org:10.1242/dmm.049571", null, "pubmed:38748804", null, "egr3 wild type siblings 2", "GSM7745909", null, "source name:Heart|tissue:Heart|genotype:bns577+/+|geo loc name:missing|collection date:missing", "egr3 wild type siblings 2", "Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q20 in a window of 20 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 2.27.1 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.2 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 raw count matrix was normalized with DESeq2 version 1.30.1 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2 and batch corrected using CountClust each biological replicate = one batch Dey K et al. Visualizing the structure of RNA seq expression data using grade of membership models. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Assembly: danRer11 Supplementary files format and content: libryr size notmalize amd batch corrected counts", "Heart", null, "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "tissue:Heart|genotype:bns577+/+", "GSM7745909", "GSM7745909: egr3 wild type siblings 2; Danio rerio; RNA Seq", "GSM7745909 r1", "GSM7745909", "1", "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP457576", null, "loader:fastq load.py", "E22_3626_Lib_Agatha_egr3_WT2_R1.fastq.gz", "fastq", 3473319384.0, 49279465.0, "GSM7745909 r1", "0:70.48", "A:943794847;C:792135324;G:792042625;T:945083925;N:262663", 70, null, null, null, 943794847, 792135324, 792042625, 945083925, 262663, "SRX21533024", "SRS18745490", "SRA1702458", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.68549, null, 0.04588, null, 0.76865, null, 0.44964, null, 71, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_plate", "smartseq", null, "Germany", "2023-08-30", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [25321, "SRR25810879", "SRX21533023", "SRS18745489", "SRP457576", "PRJNA1010780", "Effect of egr3 knockout on gene expression of dissected zebrafish hearts", "GSE241935", "Transcriptome Analysis", "To screen for Egr3 targets mediating cardiac valve development we assessed gene expression on dissected hearts of egr3 mutants and wild type siblings. Overall design: To evaluate the transcriptional differences underlying the egr3 mutant phenotype we conducted a bulk RNA seq analysis in dissected zebrafish hearts at 48 hpf. We dissected 20 hearts for each biological duplicate of egr3 mutant and wild type sibling samples in cold DMEM with 10% FBS. Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u00b5l of RNase free water. Analysis of the obtained reads confirmed the 11bp deletion in the mutant samples. 1. Boezio G. L. M. et al. The developing epicardium regulates cardiac chamber morphogenesis by promoting cardiomyocyte growth. Dis Model Mech 16 2023. https://doi.org:10.1242/dmm.049571", null, "pubmed:38748804", null, "egr3 wild type siblings 1", "GSM7745908", null, "source name:Heart|tissue:Heart|genotype:bns577+/+|geo loc name:missing|collection date:missing", "egr3 wild type siblings 1", "Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q20 in a window of 20 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 2.27.1 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.2 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 raw count matrix was normalized with DESeq2 version 1.30.1 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2 and batch corrected using CountClust each biological replicate = one batch Dey K et al. Visualizing the structure of RNA seq expression data using grade of membership models. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Assembly: danRer11 Supplementary files format and content: libryr size notmalize amd batch corrected counts", "Heart", null, "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "tissue:Heart|genotype:bns577+/+", "GSM7745908", "GSM7745908: egr3 wild type siblings 1; Danio rerio; RNA Seq", "GSM7745908 r1", "GSM7745908", "1", "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP457576", null, "loader:fastq load.py", "E22_3626_Lib_Agatha_egr3_WT1_R1.fastq.gz", "fastq", 3909248616.0, 55045571.0, "GSM7745908 r1", "0:71.02", "A:1048107387;C:905014546;G:907455489;T:1048528690;N:142504", 71, null, null, null, 1048107387, 905014546, 907455489, 1048528690, 142504, "SRX21533023", "SRS18745489", "SRA1702458", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.94958, null, 0.06298, null, 0.74819, null, 0.45762, null, 72, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_plate", "smartseq", null, "Germany", "2023-08-30", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [25322, "SRR25810880", "SRX21533022", "SRS18745488", "SRP457576", "PRJNA1010780", "Effect of egr3 knockout on gene expression of dissected zebrafish hearts", "GSE241935", "Transcriptome Analysis", "To screen for Egr3 targets mediating cardiac valve development we assessed gene expression on dissected hearts of egr3 mutants and wild type siblings. Overall design: To evaluate the transcriptional differences underlying the egr3 mutant phenotype we conducted a bulk RNA seq analysis in dissected zebrafish hearts at 48 hpf. We dissected 20 hearts for each biological duplicate of egr3 mutant and wild type sibling samples in cold DMEM with 10% FBS. Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u00b5l of RNase free water. Analysis of the obtained reads confirmed the 11bp deletion in the mutant samples. 1. Boezio G. L. M. et al. The developing epicardium regulates cardiac chamber morphogenesis by promoting cardiomyocyte growth. Dis Model Mech 16 2023. https://doi.org:10.1242/dmm.049571", null, "pubmed:38748804", null, "egr3 mutants 2", "GSM7745907", null, "source name:Heart|tissue:Heart|genotype:bns577 / |geo loc name:missing|collection date:missing", "egr3 mutants 2", "Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q20 in a window of 20 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 2.27.1 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.2 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 raw count matrix was normalized with DESeq2 version 1.30.1 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2 and batch corrected using CountClust each biological replicate = one batch Dey K et al. Visualizing the structure of RNA seq expression data using grade of membership models. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Assembly: danRer11 Supplementary files format and content: libryr size notmalize amd batch corrected counts", "Heart", null, "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "tissue:Heart|genotype:bns577 / ", "GSM7745907", "GSM7745907: egr3 mutants 2; Danio rerio; RNA Seq", "GSM7745907 r1", "GSM7745907", "1", "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP457576", null, "loader:fastq load.py", "E22_3626_Lib_Agatha_egr3_Mut2_R1.fastq.gz", "fastq", 3432675258.0, 48483287.0, "GSM7745907 r1", "0:70.80", "A:925832958;C:788551205;G:790129536;T:927993012;N:168547", 70, null, null, null, 925832958, 788551205, 790129536, 927993012, 168547, "SRX21533022", "SRS18745488", "SRA1702458", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.75652, null, 0.04046, null, 0.76455, null, 0.46333, null, 72, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_plate", "smartseq", null, "Germany", "2023-08-30", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [25323, "SRR25810881", "SRX21533021", "SRS18745487", "SRP457576", "PRJNA1010780", "Effect of egr3 knockout on gene expression of dissected zebrafish hearts", "GSE241935", "Transcriptome Analysis", "To screen for Egr3 targets mediating cardiac valve development we assessed gene expression on dissected hearts of egr3 mutants and wild type siblings. Overall design: To evaluate the transcriptional differences underlying the egr3 mutant phenotype we conducted a bulk RNA seq analysis in dissected zebrafish hearts at 48 hpf. We dissected 20 hearts for each biological duplicate of egr3 mutant and wild type sibling samples in cold DMEM with 10% FBS. Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u00b5l of RNase free water. Analysis of the obtained reads confirmed the 11bp deletion in the mutant samples. 1. Boezio G. L. M. et al. The developing epicardium regulates cardiac chamber morphogenesis by promoting cardiomyocyte growth. Dis Model Mech 16 2023. https://doi.org:10.1242/dmm.049571", null, "pubmed:38748804", null, "egr3 mutants 1", "GSM7745906", null, "source name:Heart|tissue:Heart|genotype:bns577 / |geo loc name:missing|collection date:missing", "egr3 mutants 1", "Trimmomatic version 0.39 was employed to trim reads post a quality drop below a mean of Q20 in a window of 20 nucleotides and keeping only filtered reads longer than 15 nucleotides Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 2.27.1 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.2 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 raw count matrix was normalized with DESeq2 version 1.30.1 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2 and batch corrected using CountClust each biological replicate = one batch Dey K et al. Visualizing the structure of RNA seq expression data using grade of membership models. Genes were classified as significantly differentially expressed at average count > 5 multiple testing adjusted p value < 0.05 and 0.585 < log2FC > 0.585. Assembly: danRer11 Supplementary files format and content: libryr size notmalize amd batch corrected counts", "Heart", null, "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "tissue:Heart|genotype:bns577 / ", "GSM7745906", "GSM7745906: egr3 mutants 1; Danio rerio; RNA Seq", "GSM7745906 r1", "GSM7745906", "1", "Total RNA was isolated using the miRNeasy micro Kit Qiagen 217084 followed by on column DNase digestion DNase Free DNase Set Qiagen 79254 and final elution was performed in 12\u03bcl of RNase free water 10ng total RNA was used for SMART Seq\u00ae v4 Ultra\u00ae Low Input RNA Kit Takara Bio.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP457576", null, "loader:fastq load.py", "E22_3626_Lib_Agatha_egr3_Mut1_R1.fastq.gz", "fastq", 3838969347.0, 54545950.0, "GSM7745906 r1", "0:70.38", "A:1016913415;C:902500250;G:903033204;T:1016194618;N:327860", 70, null, null, null, 1016913415, 902500250, 903033204, 1016194618, 327860, "SRX21533021", "SRS18745487", "SRA1702458", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.9511, null, 0.05017, null, 0.75341, null, 0.47152, null, 72, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_plate", "smartseq", null, "Germany", "2023-08-30", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [29201, "SRR27319715", "SRX22996941", "SRS19961590", "SRP479504", "PRJNA1055557", "Border zone cardiomyocytes and macrophages contribute to remodeling of the extracellular matrix to promote cardiomyocyte invasion during zebrafish cardiac regeneration", "GSE251856", "Other", "Despite numerous advances in our understanding of zebrafish cardiac regeneration an aspect that remains less studied is how newly proliferated cardiomyocytes invade and eventually replace the collagen containing fibrotic tissue following injury. Here we provide an in depth analysis of the process of cardiomyocyte invasion and migration using live imaging and histological approaches. We observed a close interaction between protruding cardiomyocytes and macrophages at the wound border zone and irf8 mutant zebrafish which largely lack macrophages exhibited defects in extracellular matrix ECM remodeling and cardiomyocyte protrusion into the injured area. Using a resident macrophage ablation model we show that defects in ECM remodeling at the border zone and subsequent cardiomyocyte protrusion can be partly attributed to a population of resident macrophages. Single cell RNA sequencing analysis of cells at the wound border revealed a population of cardiomyocytes and macrophages with fibroblast like gene expression signatures including the expression of genes encoding ECM structural proteins and ECM remodeling proteins. The expression of mmp14b which encodes a membrane anchored matrix metalloproteinase was restricted to cells in the border zone and genetic deletion of mmp14b led to a decrease in 1 collagen degradation at the border zone 2 macrophage recruitment to the border zone and 3 subsequent cardiomyocyte invasion. Furthermore cardiomyocyte specific overexpression of mmp14b was sufficient to enhance cardiomyocyte invasion both into the injured area and along the apical surface of the wound. Altogether our data shed important insights into the process of cardiomyocyte invasion of the collagen containing injured tissue during cardiac regeneration. They further suggest that cardiomyocytes and resident macrophages contribute to ECM remodeling at the border zone to promote cardiomyocyte replenishment of the fibrotic injured tissue. Overall design: The border zone of regenerating wild type zebrafish hearts at 7 dpci was microdissected and subjected to scRNA seq", null, "pubmed:39962064;pubmed:40268967", null, "scRNA seq of wild type border z1 cells of regenerating hearts at 7 dpci", "GSM7989198", null, "source name:Heart|tissue:Heart|genotype:Wild type|treatment:Hearts were cryoinjured and border z1 cells were microdissected at 7 dpci and pooled for scRNA seq|geo loc name:missing|collection date:missing", "scRNA seq of wild type border z1 cells of regenerating hearts at 7 dpci", "Reads were aligned against the zebrafish genome DanRer11 and counted by StarSolo. Preprocessed counts were further analysed using Scanpy. Basic cell quality control was conducted by taking the number of detected genes and mitochondrial content into consideration. We removed 23 cells in total that did not express more than 300 genes or had a mitochondrial content greater than 40%. Furthermore we filtered 9874 genes if they were detected in less than 30 cells <0.01%. Raw counts per cell were normalised to the median count over all cells and transformed into log space to stabilise variance. We initially reduced dimensionality of the dataset using PCA retaining 50 principal components. Subsequent steps like low dimensional UMAP embedding and cell clustering via community detection were based on the initial PCA. Final data visualization was done by scanpy and cellxgene packages. Assembly: danRer11 Supplementary files format and content: starsolo outputs", "Heart", "Zebrafish hearts were cryoinjured and extracted at 7 dpci.", "Border zone cells from 8 hearts were pooled and tissue dissociation was performed using the Pierce Primary Cardiomyocyte Isolation kit according to manufacturer's instructions. Cells were resuspended in DMEM with 10% FBS and 1x glutamate. The cell suspensions were depleted for dead cells using LeviCell 1.0 device Levitas Bio counted with MOX Z cell counter and diluted according to manufacturer\u2019s protocol to obtain 10.000 single cell data points per sample. Each sample was run separately on a lane in Chromium controller with Chromium Next GEM Single Cell 3\u02b9 Reagent Kits v3.1 10xGenomics. Single cell RNAseq library preparation was done using standard protocol.", null, "tissue:Heart|genotype:Wild type|treatment:Hearts were cryoinjured and border z1 cells were microdissected at 7 dpci and pooled for scRNA seq", "GSM7989198", "GSM7989198: scRNA seq of wild type border z1 cells of regenerating hearts at 7 dpci; Danio rerio; RNA Seq", "GSM7989198 r1", "GSM7989198", "1", "Border zone cells from 8 hearts were pooled and tissue dissociation was performed using the Pierce Primary Cardiomyocyte Isolation kit according to manufacturer's instructions. Cells were resuspended in DMEM with 10% FBS and 1x glutamate. The cell suspensions were depleted for dead cells using LeviCell 1.0 device Levitas Bio counted with MOX Z cell counter and diluted according to manufacturer's protocol to obtain 10.000 single cell data points per sample. Each sample was run separately on a lane in Chromium controller with Chromium Next GEM Single Cell 3\u02b9 Reagent Kits v3.1 10xGenomics. Single cell RNAseq library preparation was done using standard protocol.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "NextSeq 2000", null, "SRP479504", null, null, "Arica_10x_Zebrafish_Borderzone_Lib_R2.fastq.gz Arica_10x_Zebrafish_Borderzone_Lib_R1.fastq.gz", "fastq fastq", 35579193737.0, 447572139.0, "GSM7989198 r1", "0:28 1:51.49", "A:9662436792;C:7884457111;G:8055970010;T:9787114480;N:189215344", 28, 51, null, null, 9662436792, 7884457111, 8055970010, 9787114480, 189215344, "SRX22996941", "SRS19961590", "SRA1774131", "MPI for heart and lung research", "MPI for heart and lung research", 2, 0.00237, 0.94011, 0.00086, 0.09945, 0.99571, 0.81907, 0.32746, 0.60892, 28, 51, "T", "B", "sc-like readlen", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "Germany", "2023-12-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [29569, "SRR27368685", "SRX23045203", "SRS20006222", "SRP480346", "PRJNA1057908", "An in vivo repertoire of zebrafish cardiomyocyte specific cis regulatory elements [RNA Seq]", "GSE252151", "Transcriptome Analysis", "cis Regulatory elements cREs are essential for the spatio temporal control of gene expression during development and disease. However cRE activity is highly dependent on cell and tissue type. The developing heart is composed of several cell types predominantly cardiomyocytes. Therefore cardiomyocytes specific modelling is required to understand the cis regulation of the developing heart. Zebrafish are an ideal model to study heart development as they share a number of physiological features with the human heart during development. Therefore we present a comprehensive cardiomyocyte specific repertoire of cREs isolated from zebrafish larvae. This data combines live transcriptomics and epigenetic profiling providing insights into cREs and their associated genes involved in heart development. We further perform a transgenic reporter assay for the identified cREs of bmp10 and popdc2 genes validating these genomic regions as cardiac regulatory elements. We share this comprehensive reproducible cardiomyocyte specific cRE resource as an interrogable web tool for understanding the epigenetic and transcriptomic mechanisms underlying heart development and emergence of congenital heart defects. Overall design: Cardiomyocytes were isolated from the Tgmyl7::GFP zebrafish transgenic line. Larvae were collected 72 hpf GFP positive 30 000 cells n=3 biological replicates and GFP negative cells 500 000 cells n=3 biological replicates were collected and RNA sequencing was performed on these samples.", "parent bioproject:PRJNA1057890", null, null, "500kGFPneg6 Non cardiomyocytes", "GSM7995233", null, "source name:Heart|tissue:Heart|cell line:Primary cells|cell type:Non cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPneg|treatment:Control|geo loc name:missing|collection date:missing", "500kGFPneg6 Non cardiomyocytes", "FASTQ files were quality trimmed for overrepresented sequences using Cutadapt version 1.16 Martin 2011. The files were then processed for mapping and obtaining read counts with RNAsik Tsyganov et al 2018 using default parameters. There were two sets of counts obtained the first were the reads mapped to genome Zv9 and the second to genome Zv10. Read counts obtained from mapping to Zv10 were used for RNA seq analysis and visualizations. Read counts obtained from mapping to Zv9 were used for RNA seq analysis to obtain a set of DEGs and were then used to overlap with the genes associated to peaks of the ChIP seq data sets. Assembly: Zv9 Zv10 Supplementary files format and content: txt.gz: compressed tab delimited text files include count values for each sample", "Heart", null, "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "tissue:Heart|cell line:Primary cells|cell type:Non cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPneg|treatment:Control", "GSM7995233", "GSM7995233: 500kGFPneg6 Non cardiomyocytes; Danio rerio; RNA Seq", "GSM7995233 r1", "GSM7995233", "1", "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP480346", null, null, "500kGFPneg6_S42_L008_R1_001.fastq.gz", "fastq", 527477356.0, 10449387.0, "GSM7995233 r1", "0:50.48", "A:141759410;C:113279303;G:116384028;T:155860577;N:194038", 50, null, null, null, 141759410, 113279303, 116384028, 155860577, 194038, "SRX23045203", "SRS20006222", "SRA1776396", "Australian Regenerative Medicine Institute, Monash University", "Australian Regenerative Medicine Institute, Monash University", 1, 0.79175, null, 0.2711, null, 0.7587, null, 0.61924, null, 51, null, "B", null, "usable mapping rate", "illumina", "hiseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2023-12-27", "Undetermined", "Larval", "Heart", "Cardiovascular System"], [29570, "SRR27368686", "SRX23045202", "SRS20006221", "SRP480346", "PRJNA1057908", "An in vivo repertoire of zebrafish cardiomyocyte specific cis regulatory elements [RNA Seq]", "GSE252151", "Transcriptome Analysis", "cis Regulatory elements cREs are essential for the spatio temporal control of gene expression during development and disease. However cRE activity is highly dependent on cell and tissue type. The developing heart is composed of several cell types predominantly cardiomyocytes. Therefore cardiomyocytes specific modelling is required to understand the cis regulation of the developing heart. Zebrafish are an ideal model to study heart development as they share a number of physiological features with the human heart during development. Therefore we present a comprehensive cardiomyocyte specific repertoire of cREs isolated from zebrafish larvae. This data combines live transcriptomics and epigenetic profiling providing insights into cREs and their associated genes involved in heart development. We further perform a transgenic reporter assay for the identified cREs of bmp10 and popdc2 genes validating these genomic regions as cardiac regulatory elements. We share this comprehensive reproducible cardiomyocyte specific cRE resource as an interrogable web tool for understanding the epigenetic and transcriptomic mechanisms underlying heart development and emergence of congenital heart defects. Overall design: Cardiomyocytes were isolated from the Tgmyl7::GFP zebrafish transgenic line. Larvae were collected 72 hpf GFP positive 30 000 cells n=3 biological replicates and GFP negative cells 500 000 cells n=3 biological replicates were collected and RNA sequencing was performed on these samples.", "parent bioproject:PRJNA1057890", null, null, "500kGFPneg5 Non cardiomyocytes", "GSM7995232", null, "source name:Heart|tissue:Heart|cell line:Primary cells|cell type:Non cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPneg|treatment:Control|geo loc name:missing|collection date:missing", "500kGFPneg5 Non cardiomyocytes", "FASTQ files were quality trimmed for overrepresented sequences using Cutadapt version 1.16 Martin 2011. The files were then processed for mapping and obtaining read counts with RNAsik Tsyganov et al 2018 using default parameters. There were two sets of counts obtained the first were the reads mapped to genome Zv9 and the second to genome Zv10. Read counts obtained from mapping to Zv10 were used for RNA seq analysis and visualizations. Read counts obtained from mapping to Zv9 were used for RNA seq analysis to obtain a set of DEGs and were then used to overlap with the genes associated to peaks of the ChIP seq data sets. Assembly: Zv9 Zv10 Supplementary files format and content: txt.gz: compressed tab delimited text files include count values for each sample", "Heart", null, "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "tissue:Heart|cell line:Primary cells|cell type:Non cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPneg|treatment:Control", "GSM7995232", "GSM7995232: 500kGFPneg5 Non cardiomyocytes; Danio rerio; RNA Seq", "GSM7995232 r1", "GSM7995232", "1", "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP480346", null, null, "500kGFPneg5_S41_L008_R1_001.fastq.gz", "fastq", 3356204764.0, 66511806.0, "GSM7995232 r1", "0:50.46", "A:860342578;C:766593257;G:774473426;T:953992775;N:802728", 50, null, null, null, 860342578, 766593257, 774473426, 953992775, 802728, "SRX23045202", "SRS20006221", "SRA1776396", "Australian Regenerative Medicine Institute, Monash University", "Australian Regenerative Medicine Institute, Monash University", 1, 0.70469, null, 0.23332, null, 0.76992, null, 0.62712, null, 51, null, "B", null, "usable mapping rate", "illumina", "hiseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2023-12-27", "Undetermined", "Larval", "Heart", "Cardiovascular System"], [29571, "SRR27368687", "SRX23045201", "SRS20006220", "SRP480346", "PRJNA1057908", "An in vivo repertoire of zebrafish cardiomyocyte specific cis regulatory elements [RNA Seq]", "GSE252151", "Transcriptome Analysis", "cis Regulatory elements cREs are essential for the spatio temporal control of gene expression during development and disease. However cRE activity is highly dependent on cell and tissue type. The developing heart is composed of several cell types predominantly cardiomyocytes. Therefore cardiomyocytes specific modelling is required to understand the cis regulation of the developing heart. Zebrafish are an ideal model to study heart development as they share a number of physiological features with the human heart during development. Therefore we present a comprehensive cardiomyocyte specific repertoire of cREs isolated from zebrafish larvae. This data combines live transcriptomics and epigenetic profiling providing insights into cREs and their associated genes involved in heart development. We further perform a transgenic reporter assay for the identified cREs of bmp10 and popdc2 genes validating these genomic regions as cardiac regulatory elements. We share this comprehensive reproducible cardiomyocyte specific cRE resource as an interrogable web tool for understanding the epigenetic and transcriptomic mechanisms underlying heart development and emergence of congenital heart defects. Overall design: Cardiomyocytes were isolated from the Tgmyl7::GFP zebrafish transgenic line. Larvae were collected 72 hpf GFP positive 30 000 cells n=3 biological replicates and GFP negative cells 500 000 cells n=3 biological replicates were collected and RNA sequencing was performed on these samples.", "parent bioproject:PRJNA1057890", null, null, "500kGFPneg4 Non cardiomyocytes", "GSM7995231", null, "source name:Heart|tissue:Heart|cell line:Primary cells|cell type:Non cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPneg|treatment:Control|geo loc name:missing|collection date:missing", "500kGFPneg4 Non cardiomyocytes", "FASTQ files were quality trimmed for overrepresented sequences using Cutadapt version 1.16 Martin 2011. The files were then processed for mapping and obtaining read counts with RNAsik Tsyganov et al 2018 using default parameters. There were two sets of counts obtained the first were the reads mapped to genome Zv9 and the second to genome Zv10. Read counts obtained from mapping to Zv10 were used for RNA seq analysis and visualizations. Read counts obtained from mapping to Zv9 were used for RNA seq analysis to obtain a set of DEGs and were then used to overlap with the genes associated to peaks of the ChIP seq data sets. Assembly: Zv9 Zv10 Supplementary files format and content: txt.gz: compressed tab delimited text files include count values for each sample", "Heart", null, "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "tissue:Heart|cell line:Primary cells|cell type:Non cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPneg|treatment:Control", "GSM7995231", "GSM7995231: 500kGFPneg4 Non cardiomyocytes; Danio rerio; RNA Seq", "GSM7995231 r1", "GSM7995231", "1", "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP480346", null, null, "500kGFPneg4_S40_L008_R1_001.fastq.gz", "fastq", 3075367681.0, 60986692.0, "GSM7995231 r1", "0:50.43", "A:807059039;C:682279458;G:696326840;T:888937765;N:764579", 50, null, null, null, 807059039, 682279458, 696326840, 888937765, 764579, "SRX23045201", "SRS20006220", "SRA1776396", "Australian Regenerative Medicine Institute, Monash University", "Australian Regenerative Medicine Institute, Monash University", 1, 0.74255, null, 0.26699, null, 0.76786, null, 0.63053, null, 50, null, "B", null, "usable mapping rate", "illumina", "hiseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2023-12-27", "Undetermined", "Larval", "Heart", "Cardiovascular System"], [29572, "SRR27368688", "SRX23045200", "SRS20006219", "SRP480346", "PRJNA1057908", "An in vivo repertoire of zebrafish cardiomyocyte specific cis regulatory elements [RNA Seq]", "GSE252151", "Transcriptome Analysis", "cis Regulatory elements cREs are essential for the spatio temporal control of gene expression during development and disease. However cRE activity is highly dependent on cell and tissue type. The developing heart is composed of several cell types predominantly cardiomyocytes. Therefore cardiomyocytes specific modelling is required to understand the cis regulation of the developing heart. Zebrafish are an ideal model to study heart development as they share a number of physiological features with the human heart during development. Therefore we present a comprehensive cardiomyocyte specific repertoire of cREs isolated from zebrafish larvae. This data combines live transcriptomics and epigenetic profiling providing insights into cREs and their associated genes involved in heart development. We further perform a transgenic reporter assay for the identified cREs of bmp10 and popdc2 genes validating these genomic regions as cardiac regulatory elements. We share this comprehensive reproducible cardiomyocyte specific cRE resource as an interrogable web tool for understanding the epigenetic and transcriptomic mechanisms underlying heart development and emergence of congenital heart defects. Overall design: Cardiomyocytes were isolated from the Tgmyl7::GFP zebrafish transgenic line. Larvae were collected 72 hpf GFP positive 30 000 cells n=3 biological replicates and GFP negative cells 500 000 cells n=3 biological replicates were collected and RNA sequencing was performed on these samples.", "parent bioproject:PRJNA1057890", null, null, "30kGFPpos3 Cardiomyocytes", "GSM7995230", null, "source name:Heart|tissue:Heart|cell line:Primary cells|cell type:Cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPpos|treatment:Control|geo loc name:missing|collection date:missing", "30kGFPpos3 Cardiomyocytes", "FASTQ files were quality trimmed for overrepresented sequences using Cutadapt version 1.16 Martin 2011. The files were then processed for mapping and obtaining read counts with RNAsik Tsyganov et al 2018 using default parameters. There were two sets of counts obtained the first were the reads mapped to genome Zv9 and the second to genome Zv10. Read counts obtained from mapping to Zv10 were used for RNA seq analysis and visualizations. Read counts obtained from mapping to Zv9 were used for RNA seq analysis to obtain a set of DEGs and were then used to overlap with the genes associated to peaks of the ChIP seq data sets. Assembly: Zv9 Zv10 Supplementary files format and content: txt.gz: compressed tab delimited text files include count values for each sample", "Heart", null, "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "tissue:Heart|cell line:Primary cells|cell type:Cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPpos|treatment:Control", "GSM7995230", "GSM7995230: 30kGFPpos3 Cardiomyocytes; Danio rerio; RNA Seq", "GSM7995230 r1", "GSM7995230", "1", "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP480346", null, null, "30kGFPpos3_S39_L008_R1_001.fastq.gz", "fastq", 2938808771.0, 58361915.0, "GSM7995230 r1", "0:50.35", "A:533261626;C:883704329;G:825929620;T:694986734;N:926462", 50, null, null, null, 533261626, 883704329, 825929620, 694986734, 926462, "SRX23045200", "SRS20006219", "SRA1776396", "Australian Regenerative Medicine Institute, Monash University", "Australian Regenerative Medicine Institute, Monash University", 1, 0.12924, null, 0.05415, null, 0.92034, null, 0.70896, null, 51, null, "B", null, "usable mapping rate", "illumina", "hiseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2023-12-27", "Undetermined", "Larval", "Heart", "Cardiovascular System"], [29573, "SRR27368689", "SRX23045199", "SRS20006218", "SRP480346", "PRJNA1057908", "An in vivo repertoire of zebrafish cardiomyocyte specific cis regulatory elements [RNA Seq]", "GSE252151", "Transcriptome Analysis", "cis Regulatory elements cREs are essential for the spatio temporal control of gene expression during development and disease. However cRE activity is highly dependent on cell and tissue type. The developing heart is composed of several cell types predominantly cardiomyocytes. Therefore cardiomyocytes specific modelling is required to understand the cis regulation of the developing heart. Zebrafish are an ideal model to study heart development as they share a number of physiological features with the human heart during development. Therefore we present a comprehensive cardiomyocyte specific repertoire of cREs isolated from zebrafish larvae. This data combines live transcriptomics and epigenetic profiling providing insights into cREs and their associated genes involved in heart development. We further perform a transgenic reporter assay for the identified cREs of bmp10 and popdc2 genes validating these genomic regions as cardiac regulatory elements. We share this comprehensive reproducible cardiomyocyte specific cRE resource as an interrogable web tool for understanding the epigenetic and transcriptomic mechanisms underlying heart development and emergence of congenital heart defects. Overall design: Cardiomyocytes were isolated from the Tgmyl7::GFP zebrafish transgenic line. Larvae were collected 72 hpf GFP positive 30 000 cells n=3 biological replicates and GFP negative cells 500 000 cells n=3 biological replicates were collected and RNA sequencing was performed on these samples.", "parent bioproject:PRJNA1057890", null, null, "30kGFPpos2 Cardiomyocytes", "GSM7995229", null, "source name:Heart|tissue:Heart|cell line:Primary cells|cell type:Cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPpos|treatment:Control|geo loc name:missing|collection date:missing", "30kGFPpos2 Cardiomyocytes", "FASTQ files were quality trimmed for overrepresented sequences using Cutadapt version 1.16 Martin 2011. The files were then processed for mapping and obtaining read counts with RNAsik Tsyganov et al 2018 using default parameters. There were two sets of counts obtained the first were the reads mapped to genome Zv9 and the second to genome Zv10. Read counts obtained from mapping to Zv10 were used for RNA seq analysis and visualizations. Read counts obtained from mapping to Zv9 were used for RNA seq analysis to obtain a set of DEGs and were then used to overlap with the genes associated to peaks of the ChIP seq data sets. Assembly: Zv9 Zv10 Supplementary files format and content: txt.gz: compressed tab delimited text files include count values for each sample", "Heart", null, "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "tissue:Heart|cell line:Primary cells|cell type:Cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPpos|treatment:Control", "GSM7995229", "GSM7995229: 30kGFPpos2 Cardiomyocytes; Danio rerio; RNA Seq", "GSM7995229 r1", "GSM7995229", "1", "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP480346", null, null, "30kGFPpos2_S38_L008_R1_001.fastq.gz", "fastq", 3006409096.0, 59645543.0, "GSM7995229 r1", "0:50.40", "A:560839480;C:885691877;G:830121593;T:728932219;N:823927", 50, null, null, null, 560839480, 885691877, 830121593, 728932219, 823927, "SRX23045199", "SRS20006218", "SRA1776396", "Australian Regenerative Medicine Institute, Monash University", "Australian Regenerative Medicine Institute, Monash University", 1, 0.17805, null, 0.06115, null, 0.89769, null, 0.68731, null, 49, null, "B", null, "usable mapping rate", "illumina", "hiseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2023-12-27", "Undetermined", "Larval", "Heart", "Cardiovascular System"], [29574, "SRR27368690", "SRX23045198", "SRS20006217", "SRP480346", "PRJNA1057908", "An in vivo repertoire of zebrafish cardiomyocyte specific cis regulatory elements [RNA Seq]", "GSE252151", "Transcriptome Analysis", "cis Regulatory elements cREs are essential for the spatio temporal control of gene expression during development and disease. However cRE activity is highly dependent on cell and tissue type. The developing heart is composed of several cell types predominantly cardiomyocytes. Therefore cardiomyocytes specific modelling is required to understand the cis regulation of the developing heart. Zebrafish are an ideal model to study heart development as they share a number of physiological features with the human heart during development. Therefore we present a comprehensive cardiomyocyte specific repertoire of cREs isolated from zebrafish larvae. This data combines live transcriptomics and epigenetic profiling providing insights into cREs and their associated genes involved in heart development. We further perform a transgenic reporter assay for the identified cREs of bmp10 and popdc2 genes validating these genomic regions as cardiac regulatory elements. We share this comprehensive reproducible cardiomyocyte specific cRE resource as an interrogable web tool for understanding the epigenetic and transcriptomic mechanisms underlying heart development and emergence of congenital heart defects. Overall design: Cardiomyocytes were isolated from the Tgmyl7::GFP zebrafish transgenic line. Larvae were collected 72 hpf GFP positive 30 000 cells n=3 biological replicates and GFP negative cells 500 000 cells n=3 biological replicates were collected and RNA sequencing was performed on these samples.", "parent bioproject:PRJNA1057890", null, null, "30kGFPpos1 Cardiomyocytes", "GSM7995228", null, "source name:Heart|tissue:Heart|cell line:Primary cells|cell type:Cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPpos|treatment:Control|geo loc name:missing|collection date:missing", "30kGFPpos1 Cardiomyocytes", "FASTQ files were quality trimmed for overrepresented sequences using Cutadapt version 1.16 Martin 2011. The files were then processed for mapping and obtaining read counts with RNAsik Tsyganov et al 2018 using default parameters. There were two sets of counts obtained the first were the reads mapped to genome Zv9 and the second to genome Zv10. Read counts obtained from mapping to Zv10 were used for RNA seq analysis and visualizations. Read counts obtained from mapping to Zv9 were used for RNA seq analysis to obtain a set of DEGs and were then used to overlap with the genes associated to peaks of the ChIP seq data sets. Assembly: Zv9 Zv10 Supplementary files format and content: txt.gz: compressed tab delimited text files include count values for each sample", "Heart", null, "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "tissue:Heart|cell line:Primary cells|cell type:Cardiomyocytes|genotype:Tgmyl7::GFP|gfp status:GFPpos|treatment:Control", "GSM7995228", "GSM7995228: 30kGFPpos1 Cardiomyocytes; Danio rerio; RNA Seq", "GSM7995228 r1", "GSM7995228", "1", "RNA extraction was performed using the RNEasy Plus Micro Kit Qiagen according to the instructions provided in the manual. Integrity of the extracted RNA was assessed with BioAnalyzer Agilent and the concentration was measured with Qubit Q32866 Qubit\u2122 RNA HS Assay Kit Q32852 ThermoFisher Scientific. RNA libraries were prepared for sequencing using standard Illumina protocols", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP480346", null, null, "30kGFPpos1_S37_L008_R1_001.fastq.gz", "fastq", 3254639839.0, 64665631.0, "GSM7995228 r1", "0:50.33", "A:545193535;C:1023804678;G:938318027;T:746302007;N:1021592", 50, null, null, null, 545193535, 1023804678, 938318027, 746302007, 1021592, "SRX23045198", "SRS20006217", "SRA1776396", "Australian Regenerative Medicine Institute, Monash University", "Australian Regenerative Medicine Institute, Monash University", 1, 0.05453, null, 0.01921, null, 0.9643, null, 0.78064, null, 49, null, "B", null, "usable mapping rate", "illumina", "hiseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Australia", "2023-12-27", "Undetermined", "Larval", "Heart", "Cardiovascular System"], [30512, "SRR27764782", "SRX23429747", "SRS20284188", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle cox7a1 / replicate 4", "GSM8042779", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle cox7a1 / replicate 4", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury", "GSM8042779", "GSM8042779: Cardiac ventricle cox7a1 / replicate 4; Danio rerio; RNA Seq", "GSM8042779 r1", "GSM8042779", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "KO_10_Directional_S8_R1_001.fastq.gz", "fastq", 8619450300.0, 86194503.0, "GSM8042779 r1", "0:100", "A:2183264320;C:2042597849;G:2002385828;T:2389908983;N:1293320", 100, null, null, null, 2183264320, 2042597849, 2002385828, 2389908983, 1293320, "SRX23429747", "SRS20284188", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30513, "SRR27764783", "SRX23429746", "SRS20284187", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle cox7a1 / replicate 3", "GSM8042778", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle cox7a1 / replicate 3", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury", "GSM8042778", "GSM8042778: Cardiac ventricle cox7a1 / replicate 3; Danio rerio; RNA Seq", "GSM8042778 r1", "GSM8042778", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "KO_9_Directional_S7_R1_001.fastq.gz", "fastq", 6466746100.0, 64667461.0, "GSM8042778 r1", "0:100", "A:1708351950;C:1464168743;G:1452219209;T:1841033764;N:972434", 100, null, null, null, 1708351950, 1464168743, 1452219209, 1841033764, 972434, "SRX23429746", "SRS20284187", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30514, "SRR27764784", "SRX23429745", "SRS20284186", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle cox7a1 / replicate 2", "GSM8042777", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle cox7a1 / replicate 2", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury", "GSM8042777", "GSM8042777: Cardiac ventricle cox7a1 / replicate 2; Danio rerio; RNA Seq", "GSM8042777 r1", "GSM8042777", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "KO_8_Directional_S6_R1_001.fastq.gz", "fastq", 6766795300.0, 67667953.0, "GSM8042777 r1", "0:100", "A:1803038642;C:1540664299;G:1518741633;T:1903355305;N:995421", 100, null, null, null, 1803038642, 1540664299, 1518741633, 1903355305, 995421, "SRX23429745", "SRS20284186", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30515, "SRR27764785", "SRX23429744", "SRS20284185", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle cox7a1 / replicate 1", "GSM8042776", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle cox7a1 / replicate 1", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:Cox7a mut|treatment:7days post cryoinjury", "GSM8042776", "GSM8042776: Cardiac ventricle cox7a1 / replicate 1; Danio rerio; RNA Seq", "GSM8042776 r1", "GSM8042776", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "KO_7_Directional_S5_R1_001.fastq.gz", "fastq", 5583049300.0, 55830493.0, "GSM8042776 r1", "0:100", "A:1479820662;C:1265599242;G:1251078421;T:1585727832;N:823143", 100, null, null, null, 1479820662, 1265599242, 1251078421, 1585727832, 823143, "SRX23429744", "SRS20284185", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30516, "SRR27764786", "SRX23429743", "SRS20284184", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle wt sibling replicate 4", "GSM8042775", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle wt sibling replicate 4", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury", "GSM8042775", "GSM8042775: Cardiac ventricle wt sibling replicate 4; Danio rerio; RNA Seq", "GSM8042775 r1", "GSM8042775", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "WT_5_Directional_S4_R1_001.fastq.gz", "fastq", 6851217800.0, 68512178.0, "GSM8042775 r1", "0:100", "A:1837112549;C:1539284911;G:1515596368;T:1958221274;N:1002698", 100, null, null, null, 1837112549, 1539284911, 1515596368, 1958221274, 1002698, "SRX23429743", "SRS20284184", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30517, "SRR27764787", "SRX23429742", "SRS20284183", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle wt sibling replicate 3", "GSM8042774", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle wt sibling replicate 3", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury", "GSM8042774", "GSM8042774: Cardiac ventricle wt sibling replicate 3; Danio rerio; RNA Seq", "GSM8042774 r1", "GSM8042774", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "WT_3_Directional_S3_R1_001.fastq.gz", "fastq", 7036251700.0, 70362517.0, "GSM8042774 r1", "0:100", "A:1881612688;C:1574593657;G:1570342252;T:2008668471;N:1034632", 100, null, null, null, 1881612688, 1574593657, 1570342252, 2008668471, 1034632, "SRX23429742", "SRS20284183", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30518, "SRR27764788", "SRX23429741", "SRS20284182", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle wt sibling replicate 2", "GSM8042773", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle wt sibling replicate 2", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury", "GSM8042773", "GSM8042773: Cardiac ventricle wt sibling replicate 2; Danio rerio; RNA Seq", "GSM8042773 r1", "GSM8042773", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "WT_2_Directional_S2_R1_001.fastq.gz", "fastq", 6856428200.0, 68564282.0, "GSM8042773 r1", "0:100", "A:1790369167;C:1572129686;G:1566120109;T:1926782247;N:1026991", 100, null, null, null, 1790369167, 1572129686, 1566120109, 1926782247, 1026991, "SRX23429741", "SRS20284182", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30519, "SRR27764789", "SRX23429740", "SRS20284181", "SRP486526", "PRJNA1070616", "Cox7a1 mediated CIV dimerization impacts skeletal muscle physiology and cardiac injury response", "GSE254466", "Transcriptome Analysis", "The oxidative phosphorylation OXPHOS system is dynamic and the respiratory complexes RCs coexist with super assembled quaternary structures called supercomplexes SCs. How assembly occurs and the physiological role of supercomplex assembly is still under intensive investigation. The Cox7a family member Cox7a2l also known as Scaf1 promotes CIII CIV super assembly and energetic efficiency in zebrafish mice and humans. Here we studied the role of a second member of the Cox7a family Cox7a1 in SC assembly and striated muscle physiology. We found that this protein drives CIV homodimer formation which increases CIV activity. The substantial reduction in CIV2 formation led to a profound metabolic rearrangement with a consequent non pathological loss of skeletal muscle performance. Ablation of Cox7a1 also rewired heart metabolism. Already in homeostatic conditions cox7a1 / hearts revealed a pro regenerative metabolic profile. While overall cardiac function was not affected the absence of Cox7a1 altered the cardiac regenerative response. The effects of cox7a1 and cox7a2l loss of function on skeletal muscle and myocardium physiology and injury response were not identical revealing that there is a high specificity of Cox7a isoform in controlling OXPHOS assembly and striated muscle metabolism. While in both cases overall OXPHOS activity is modified the loss of CIII CIV heterodimer formation or CIV homodimer formation have very distinct metabolic and physiological consequences highlighting the complexity of OXPHOS function and the importance of cox7a1 in striated muscle maturation. Overall design: Adult zebrafish hearts for cox7a1 / mutants and wildtype siblings were cryoinjured. 7 xxx post injury the cardiac ventrilces were extracted and RNA was extracted for RNA seq. 4 pools each comprising 5 ventricles were sequenced per condition.", null, "pubmed:38701784", null, "Cardiac ventricle wt sibling replicate 1", "GSM8042772", null, "source name:Cardiac Ventricle|tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury|geo loc name:missing|collection date:missing", "Cardiac ventricle wt sibling replicate 1", "Data were quality checked with Fastqc and Multiqc Sequences were trimmed with fastp 2 pass alignment was performed with STAR Aligner reads were dounted using featurecounts Normalization and downstream analysis including differential expression analysis was performed in R Assembly: GRCz11 v109 Ensembl Supplementary files format and content: feature counts tab seprated values", "Cardiac Ventricle", null, "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "tissue:Cardiac Ventricle|genotype:WT|treatment:7days post cryoinjury", "GSM8042772", "GSM8042772: Cardiac ventricle wt sibling replicate 1; Danio rerio; RNA Seq", "GSM8042772 r1", "GSM8042772", "1", "4 pools each comprising 5 ventricles were sequenced per condition. Libraries for RNA seq were prepared using the \"NEBNext Ultra II Directional RNA library prep Kit for Illumina\" following manufacturer\u00b4s protocol", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP486526", null, null, "WT_1_Directional_S1_R1_001.fastq.gz", "fastq", 7089416800.0, 70894168.0, "GSM8042772 r1", "0:100", "A:1855346146;C:1626812736;G:1599932420;T:2006283874;N:1041624", 100, null, null, null, 1855346146, 1626812736, 1599932420, 2006283874, 1041624, "SRX23429740", "SRS20284181", "SRA1793874", "University of Bern", "University of Bern", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "nebnext", "bulk", "unknown", "unknown", null, "Switzerland", "2024-01-29", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30746, "SRR28348607", "SRX23954674", "SRS20755104", "SRP495302", "PRJNA1088122", "Decoding the molecular cellular and functional heterogeneity of zebrafish intracardiac nervous system", "GSE261619", "Transcriptome Analysis", "In this project we present a comprehensive taxonomy of the intracardiac nervous system IcNS utilizing single cell RNA sequencing anatomical studies and electrophysiological techniques. Overall design: For single cell sequencing experiments 25 Tgelavl3:eGFP previously known as HuC:GFP of 5 mpf animal were used from both sexes for the first set and 25 Tgelavl3:eGFP of 11 mpf and 10 Tgnbt:DsRed of 22 mpf animals from both sexes were used for the second set. Cells were dissociated sorted by FACS as described Cosacak et al. 2019. The single cell encapsulation and cDNA synthesis done by following 10X Genomics' workflows. The reads were aligned to zebrafish genome GRChZ 11 v 105 was used for gene annotation and assigning reads to genes. Cellranger software version 6.1.2 was used to process the data.", null, "pubmed:39632839", null, "Tgelavl3:eGFP Tgnbt:DsRed", "GSM8147512", null, "source name:atrium|tissue:atrium|genotype:Tgelavl3:eGFP Tgnbt:DsRed|geo loc name:missing|collection date:missing", "Tgelavl3:eGFP Tgnbt:DsRed", "The demultiplexing barcoded processing gene counting and aggregation were made using the 10x genomics' cellranger software version 6.1.2 https://support.10xgenomics.com/single cell gene expression/software/pipelines/latest/output/metrics The fastq files were aligned to zebrafish genome GRCz11 and ensemble transcripts from Ensembl Release 105 by using STAR. The BAM files were as input for Cell Ranger 10X genomics to generate processed data files that include gene names row names and cell names column names and counts. Further analysis done by using Seurat package in R. Assembly: GRCz11 Supplementary files format and content: filtered bc matrix outputs from Cell Ranger", "atrium", null, "Cells from zebrafish heart were dissociated. In addition to GFP and DsRed in the genome of the fish viability indicator dyes Sytox Blue Invitrogen Cat No. S34857 and Dycle Ruby Invitrogen Cat. No. V10309 were used to sort the cells by FACS. The library preparation was performed by 10X Genomics as per manufacture's protocol. 10X genomics", "Zebrafish were kept in the re circulating system on a 14/10 h light/dark cycle pH7.5 at 28\u00b0C \u00b11\u00b0C in groups of 20 animals per 2.8L.", "tissue:atrium|genotype:Tgelavl3:eGFP Tgnbt:DsRed", "GSM8147512", "GSM8147512: Tgelavl3:eGFP Tgnbt:DsRed; Danio rerio; RNA Seq", "GSM8147512 r1", "GSM8147512", "1", "Cells from zebrafish heart were dissociated. In addition to GFP and DsRed in the genome of the fish viability indicator dyes Sytox Blue Invitrogen Cat No. S34857 and Dycle Ruby Invitrogen Cat. No. V10309 were used to sort the cells by FACS. The library preparation was performed by 10X Genomics as per manufacture's protocol. 10X genomics", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "NextSeq 500", null, "SRP495302", null, "loader:fastq load.py", "CP030_S1_L004_I1_001.fastq.gz CP030_S1_L004_I2_001.fastq.gz CP030_S1_L004_R1_001.fastq.gz CP030_S1_L004_R2_001.fastq.gz", "fastq fastq fastq fastq", 86914563102.0, 391507041.0, "GSM8147512 r1", "0:10 1:10 2:101 3:101", "A:23707102309;C:15625825731;G:14915197158;T:24834868356;N:1428728", 10, 10, 101, 101, 23707102309, 15625825731, 14915197158, 24834868356, 1428728, "SRX23954674", "SRS20755104", "SRA1824602", "Neurology & TAUB Institute, Columbia University", "Neurology & TAUB Institute, Columbia University", 2, 0.0, 0.94374, 0.0, 0.12308, 1.0, 0.82055, null, 0.55544, 101, 101, "T", "B", "mate1 technical by mapping diff", "illumina", "nextseq", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-03-14", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30747, "SRR28348608", "SRX23954673", "SRS20755103", "SRP495302", "PRJNA1088122", "Decoding the molecular cellular and functional heterogeneity of zebrafish intracardiac nervous system", "GSE261619", "Transcriptome Analysis", "In this project we present a comprehensive taxonomy of the intracardiac nervous system IcNS utilizing single cell RNA sequencing anatomical studies and electrophysiological techniques. Overall design: For single cell sequencing experiments 25 Tgelavl3:eGFP previously known as HuC:GFP of 5 mpf animal were used from both sexes for the first set and 25 Tgelavl3:eGFP of 11 mpf and 10 Tgnbt:DsRed of 22 mpf animals from both sexes were used for the second set. Cells were dissociated sorted by FACS as described Cosacak et al. 2019. The single cell encapsulation and cDNA synthesis done by following 10X Genomics' workflows. The reads were aligned to zebrafish genome GRChZ 11 v 105 was used for gene annotation and assigning reads to genes. Cellranger software version 6.1.2 was used to process the data.", null, "pubmed:39632839", null, "Tgelavl3:eGFP", "GSM8147511", null, "source name:whole heart|tissue:whole heart|genotype:Tgelavl3:eGFP|geo loc name:missing|collection date:missing", "Tgelavl3:eGFP", "The demultiplexing barcoded processing gene counting and aggregation were made using the 10x genomics' cellranger software version 6.1.2 https://support.10xgenomics.com/single cell gene expression/software/pipelines/latest/output/metrics The fastq files were aligned to zebrafish genome GRCz11 and ensemble transcripts from Ensembl Release 105 by using STAR. The BAM files were as input for Cell Ranger 10X genomics to generate processed data files that include gene names row names and cell names column names and counts. Further analysis done by using Seurat package in R. Assembly: GRCz11 Supplementary files format and content: filtered bc matrix outputs from Cell Ranger", "whole heart", null, "Cells from zebrafish heart were dissociated. In addition to GFP and DsRed in the genome of the fish viability indicator dyes Sytox Blue Invitrogen Cat No. S34857 and Dycle Ruby Invitrogen Cat. No. V10309 were used to sort the cells by FACS. The library preparation was performed by 10X Genomics as per manufacture's protocol. 10X genomics", "Zebrafish were kept in the re circulating system on a 14/10 h light/dark cycle pH7.5 at 28\u00b0C \u00b11\u00b0C in groups of 20 animals per 2.8L.", "tissue:whole heart|genotype:Tgelavl3:eGFP", "GSM8147511", "GSM8147511: Tgelavl3:eGFP; Danio rerio; RNA Seq", "GSM8147511 r1", "GSM8147511", "1", "Cells from zebrafish heart were dissociated. In addition to GFP and DsRed in the genome of the fish viability indicator dyes Sytox Blue Invitrogen Cat No. S34857 and Dycle Ruby Invitrogen Cat. No. V10309 were used to sort the cells by FACS. The library preparation was performed by 10X Genomics as per manufacture's protocol. 10X genomics", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "NextSeq 500", null, "SRP495302", null, "loader:fastq load.py", "CP017_S1_L001_I1_001.fastq.gz CP017_S1_L001_I2_001.fastq.gz CP017_S1_L001_R1_001.fastq.gz CP017_S1_L001_R2_001.fastq.gz", "fastq fastq fastq fastq", 41176621272.0, 185480276.0, "GSM8147511 r1", "0:10 1:10 2:101 3:101", "A:9993088511;C:6520920913;G:6513822557;T:14438876590;N:307181", 10, 10, 101, 101, 9993088511, 6520920913, 6513822557, 14438876590, 307181, "SRX23954673", "SRS20755103", "SRA1824602", "Neurology & TAUB Institute, Columbia University", "Neurology & TAUB Institute, Columbia University", 2, 0.01251, 0.96696, 0.0018, 0.07994, 0.9922, 0.83861, 0.46366, 0.47886, 101, 101, "T", "B", "mate1 technical by mapping diff", "illumina", "nextseq", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-03-14", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [30748, "SRR28348609", "SRX23954673", "SRS20755103", "SRP495302", "PRJNA1088122", "Decoding the molecular cellular and functional heterogeneity of zebrafish intracardiac nervous system", "GSE261619", "Transcriptome Analysis", "In this project we present a comprehensive taxonomy of the intracardiac nervous system IcNS utilizing single cell RNA sequencing anatomical studies and electrophysiological techniques. Overall design: For single cell sequencing experiments 25 Tgelavl3:eGFP previously known as HuC:GFP of 5 mpf animal were used from both sexes for the first set and 25 Tgelavl3:eGFP of 11 mpf and 10 Tgnbt:DsRed of 22 mpf animals from both sexes were used for the second set. Cells were dissociated sorted by FACS as described Cosacak et al. 2019. The single cell encapsulation and cDNA synthesis done by following 10X Genomics' workflows. The reads were aligned to zebrafish genome GRChZ 11 v 105 was used for gene annotation and assigning reads to genes. Cellranger software version 6.1.2 was used to process the data.", null, "pubmed:39632839", null, "Tgelavl3:eGFP", "GSM8147511", null, "source name:whole heart|tissue:whole heart|genotype:Tgelavl3:eGFP|geo loc name:missing|collection date:missing", "Tgelavl3:eGFP", "The demultiplexing barcoded processing gene counting and aggregation were made using the 10x genomics' cellranger software version 6.1.2 https://support.10xgenomics.com/single cell gene expression/software/pipelines/latest/output/metrics The fastq files were aligned to zebrafish genome GRCz11 and ensemble transcripts from Ensembl Release 105 by using STAR. The BAM files were as input for Cell Ranger 10X genomics to generate processed data files that include gene names row names and cell names column names and counts. Further analysis done by using Seurat package in R. Assembly: GRCz11 Supplementary files format and content: filtered bc matrix outputs from Cell Ranger", "whole heart", null, "Cells from zebrafish heart were dissociated. In addition to GFP and DsRed in the genome of the fish viability indicator dyes Sytox Blue Invitrogen Cat No. S34857 and Dycle Ruby Invitrogen Cat. No. V10309 were used to sort the cells by FACS. The library preparation was performed by 10X Genomics as per manufacture's protocol. 10X genomics", "Zebrafish were kept in the re circulating system on a 14/10 h light/dark cycle pH7.5 at 28\u00b0C \u00b11\u00b0C in groups of 20 animals per 2.8L.", "tissue:whole heart|genotype:Tgelavl3:eGFP", "GSM8147511", "GSM8147511: Tgelavl3:eGFP; Danio rerio; RNA Seq", "GSM8147511 r1", "GSM8147511", "1", "Cells from zebrafish heart were dissociated. In addition to GFP and DsRed in the genome of the fish viability indicator dyes Sytox Blue Invitrogen Cat No. S34857 and Dycle Ruby Invitrogen Cat. No. V10309 were used to sort the cells by FACS. The library preparation was performed by 10X Genomics as per manufacture's protocol. 10X genomics", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "NextSeq 500", null, "SRP495302", null, "loader:fastq load.py", "CP017_S1_L002_I1_001.fastq.gz CP017_S1_L002_I2_001.fastq.gz CP017_S1_L002_R1_001.fastq.gz CP017_S1_L002_R2_001.fastq.gz", "fastq fastq fastq fastq", 41449667730.0, 186710215.0, "GSM8147511 r2", "0:10 1:10 2:101 3:101", "A:10111586707;C:6536521889;G:6498472573;T:14568538148;N:344113", 10, 10, 101, 101, 10111586707, 6536521889, 6498472573, 14568538148, 344113, "SRX23954673", "SRS20755103", "SRA1824602", "Neurology & TAUB Institute, Columbia University", "Neurology & TAUB Institute, Columbia University", 2, 0.01136, 0.96721, 0.00127, 0.07919, 0.99299, 0.83956, 0.4846, 0.4789, 101, 101, "T", "B", "mate1 technical by mapping diff", "illumina", "nextseq", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-03-14", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88+/+ 24 hpci 2", "GSM8159071", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 660213492, 527347733, 572126573, 694765347, 192831, "SRX24015869", "SRS20810998", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88+/+ 1 hpci 2", "GSM8159070", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 713621237, 556223861, 630990745, 773686189, 132510, "SRX24015868", "SRS20810997", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "ventricle myd88+/+ untouched 2", "GSM8159069", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 560190602, 446185315, 485011548, 601082958, 161983, "SRX24015867", "SRS20810996", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88+/+ 24 hpci 1", "GSM8159068", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 290655996, 222128471, 247491826, 299784598, 87219, "SRX24015866", "SRS20810995", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88+/+ 1 hpci 1", "GSM8159067", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 689702458, 551265040, 603307580, 750425733, 85213, "SRX24015865", "SRS20810994", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "ventricle myd88+/+ untouched 1", "GSM8159066", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 562046544, 458761205, 496224794, 606313940, 169522, "SRX24015864", "SRS20810993", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88 / 24 hpci 2", "GSM8159065", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 669128241, 547606289, 587771598, 704439682, 197535, "SRX24015863", "SRS20810992", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88 / 1 hpci 2", "GSM8159064", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 690941775, 542509296, 605002938, 746301098, 92078, "SRX24015862", "SRS20810991", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "ventricle myd88 / untouched 2", "GSM8159063", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 588370831, 457110464, 507924919, 624586577, 171985, "SRX24015861", "SRS20810990", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88 / 24 hpci 1", "GSM8159062", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 621931320, 501998000, 541224122, 657957821, 186991, "SRX24015860", "SRS20810989", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "injured tissue myd88 / 1 hpci 1", "GSM8159061", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 679380332, 554919862, 604907160, 746451941, 77570, "SRX24015859", "SRS20810988", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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", null, "ventricle myd88 / untouched 1", "GSM8159060", null, "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\u2019s protocol Vazyme.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP497025", null, "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, null, null, null, 623574024, 490503071, 538918126, 667825381, 187098, "SRX24015858", "SRS20810987", "SRA1830778", "MPI for heart and lung research", "MPI for heart and lung research", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "Germany", "2024-03-21", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31545, "SRR28435452", "SRX24039370", "SRS20832135", "SRP497581", "PRJNA1091566", "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration", "GSE262351", "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: Aim: Investigation of the MyD88 signaling in endocardial cells during zebrafish cardiac regeneration. Methods: Endocardial cells sorted from the ETkrt4:EGFPsqet33 1A line at 96 hours post cryoinjury hpci. Conditions: 3 myd88+/+ and 3 myd88 / samples", null, "pubmed:39271818", null, "myd88 3", "GSM8163706", null, "tissue:endocardial|cell type:endocardial|genotype:myd88 / |time:96 hpci|geo loc name:missing|collection date:missing", "myd88 3", "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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 109 with STAR 2.7.10a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Assembly: danRer11 Supplementary files format and content: The tab delimited matrix shows DESeq normalized gene counts.", "endocardial", null, "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "cell type:endocardial|genotype:myd88 / |time:96 hpci", "GSM8163706", "GSM8163706: myd88 3; Danio rerio; RNA Seq", "GSM8163706 r1", "GSM8163706", "1", "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina HiSeq 4000", null, "SRP497581", null, "loader:fastq load.py", "myd88_3_1.fq.gz myd88_3_2.fq.gz", "fastq fastq", 6626254800.0, 22087516.0, "GSM8163706 r1", "0:150 1:150", "A:1858405504;C:1462442884;G:1470757827;T:1834548220;N:100365", 150, 150, null, null, 1858405504, 1462442884, 1470757827, 1834548220, 100365, "SRX24039370", "SRS20832135", "SRA1832826", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "random_priming", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-03-25", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31546, "SRR28435455", "SRX24039369", "SRS20832134", "SRP497581", "PRJNA1091566", "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration", "GSE262351", "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: Aim: Investigation of the MyD88 signaling in endocardial cells during zebrafish cardiac regeneration. Methods: Endocardial cells sorted from the ETkrt4:EGFPsqet33 1A line at 96 hours post cryoinjury hpci. Conditions: 3 myd88+/+ and 3 myd88 / samples", null, "pubmed:39271818", null, "myd88 2", "GSM8163705", null, "tissue:endocardial|cell type:endocardial|genotype:myd88 / |time:96 hpci|geo loc name:missing|collection date:missing", "myd88 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 109 with STAR 2.7.10a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Assembly: danRer11 Supplementary files format and content: The tab delimited matrix shows DESeq normalized gene counts.", "endocardial", null, "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "cell type:endocardial|genotype:myd88 / |time:96 hpci", "GSM8163705", "GSM8163705: myd88 2; Danio rerio; RNA Seq", "GSM8163705 r1", "GSM8163705", "1", "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina HiSeq 4000", null, "SRP497581", null, "loader:fastq load.py", "myd88_2_1.fq.gz myd88_2_2.fq.gz", "fastq fastq", 6586163100.0, 21953877.0, "GSM8163705 r1", "0:150 1:150", "A:1856129657;C:1440403994;G:1451543521;T:1837982507;N:103421", 150, 150, null, null, 1856129657, 1440403994, 1451543521, 1837982507, 103421, "SRX24039369", "SRS20832134", "SRA1832826", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "random_priming", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-03-25", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31547, "SRR28435453", "SRX24039368", "SRS20832133", "SRP497581", "PRJNA1091566", "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration", "GSE262351", "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: Aim: Investigation of the MyD88 signaling in endocardial cells during zebrafish cardiac regeneration. Methods: Endocardial cells sorted from the ETkrt4:EGFPsqet33 1A line at 96 hours post cryoinjury hpci. Conditions: 3 myd88+/+ and 3 myd88 / samples", null, "pubmed:39271818", null, "myd88 1", "GSM8163704", null, "tissue:endocardial|cell type:endocardial|genotype:myd88 / |time:96 hpci|geo loc name:missing|collection date:missing", "myd88 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 109 with STAR 2.7.10a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Assembly: danRer11 Supplementary files format and content: The tab delimited matrix shows DESeq normalized gene counts.", "endocardial", null, "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "cell type:endocardial|genotype:myd88 / |time:96 hpci", "GSM8163704", "GSM8163704: myd88 1; Danio rerio; RNA Seq", "GSM8163704 r1", "GSM8163704", "1", "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina HiSeq 4000", null, "SRP497581", null, "loader:fastq load.py", "myd88_1_1.fq.gz myd88_1_2.fq.gz", "fastq fastq", 6586212900.0, 21954043.0, "GSM8163704 r1", "0:150 1:150", "A:1835825607;C:1467677697;G:1474870953;T:1807740616;N:98027", 150, 150, null, null, 1835825607, 1467677697, 1474870953, 1807740616, 98027, "SRX24039368", "SRS20832133", "SRA1832826", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "random_priming", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-03-25", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31548, "SRR28435454", "SRX24039367", "SRS20832132", "SRP497581", "PRJNA1091566", "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration", "GSE262351", "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: Aim: Investigation of the MyD88 signaling in endocardial cells during zebrafish cardiac regeneration. Methods: Endocardial cells sorted from the ETkrt4:EGFPsqet33 1A line at 96 hours post cryoinjury hpci. Conditions: 3 myd88+/+ and 3 myd88 / samples", null, "pubmed:39271818", null, "WT 3", "GSM8163703", null, "tissue:endocardial|cell type:endocardial|genotype:myd88+/+|time:96 hpci|geo loc name:missing|collection date:missing", "WT 3", "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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 109 with STAR 2.7.10a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Assembly: danRer11 Supplementary files format and content: The tab delimited matrix shows DESeq normalized gene counts.", "endocardial", null, "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "cell type:endocardial|genotype:myd88+/+|time:96 hpci", "GSM8163703", "GSM8163703: WT 3; Danio rerio; RNA Seq", "GSM8163703 r1", "GSM8163703", "1", "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina HiSeq 4000", null, "SRP497581", null, "loader:fastq load.py", "WT_3_1.fq.gz WT_3_2.fq.gz", "fastq fastq", 6554345400.0, 21847818.0, "GSM8163703 r1", "0:150 1:150", "A:1829151207;C:1459298563;G:1466145928;T:1799650897;N:98805", 150, 150, null, null, 1829151207, 1459298563, 1466145928, 1799650897, 98805, "SRX24039367", "SRS20832132", "SRA1832826", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "random_priming", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-03-25", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31549, "SRR28435456", "SRX24039366", "SRS20832131", "SRP497581", "PRJNA1091566", "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration", "GSE262351", "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: Aim: Investigation of the MyD88 signaling in endocardial cells during zebrafish cardiac regeneration. Methods: Endocardial cells sorted from the ETkrt4:EGFPsqet33 1A line at 96 hours post cryoinjury hpci. Conditions: 3 myd88+/+ and 3 myd88 / samples", null, "pubmed:39271818", null, "WT 2", "GSM8163702", null, "tissue:endocardial|cell type:endocardial|genotype:myd88+/+|time:96 hpci|geo loc name:missing|collection date:missing", "WT 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 109 with STAR 2.7.10a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Assembly: danRer11 Supplementary files format and content: The tab delimited matrix shows DESeq normalized gene counts.", "endocardial", null, "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "cell type:endocardial|genotype:myd88+/+|time:96 hpci", "GSM8163702", "GSM8163702: WT 2; Danio rerio; RNA Seq", "GSM8163702 r1", "GSM8163702", "1", "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina HiSeq 4000", null, "SRP497581", null, "loader:fastq load.py", "WT_2_1.fq.gz WT_2_2.fq.gz", "fastq fastq", 6440692500.0, 21468975.0, "GSM8163702 r1", "0:150 1:150", "A:1797022330;C:1433189990;G:1440263369;T:1770115464;N:101347", 150, 150, null, null, 1797022330, 1433189990, 1440263369, 1770115464, 101347, "SRX24039366", "SRS20832131", "SRA1832826", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "random_priming", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-03-25", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31550, "SRR28435457", "SRX24039365", "SRS20832130", "SRP497581", "PRJNA1091566", "The innate immune regulator MyD88 dampens fibrosis during zebrafish heart regeneration", "GSE262351", "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: Aim: Investigation of the MyD88 signaling in endocardial cells during zebrafish cardiac regeneration. Methods: Endocardial cells sorted from the ETkrt4:EGFPsqet33 1A line at 96 hours post cryoinjury hpci. Conditions: 3 myd88+/+ and 3 myd88 / samples", null, "pubmed:39271818", null, "WT 1", "GSM8163701", null, "tissue:endocardial|cell type:endocardial|genotype:myd88+/+|time:96 hpci|geo loc name:missing|collection date:missing", "WT 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 109 with STAR 2.7.10a Dobin et al. STAR: ultrafast universal RNA seq aligner. Alignments were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 Love et al. Moderated estimation of fold change and dispersion for RNA Seq data with DESeq2. Assembly: danRer11 Supplementary files format and content: The tab delimited matrix shows DESeq normalized gene counts.", "endocardial", null, "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "cell type:endocardial|genotype:myd88+/+|time:96 hpci", "GSM8163701", "GSM8163701: WT 1; Danio rerio; RNA Seq", "GSM8163701 r1", "GSM8163701", "1", "RNA was isolated from FACS sorted endocardial cells from a pool of 4 ETkrt4:EGFP; myd88+/+ and 4 ETkrt4:EGFP; myd88 / ventricles for each sample using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase free DNase set Qiagen to avoid contamination by genomic DNA. Messenger RNA was purified from total RNA using poly T oligo attached magnetic beads. post fragmentation the first strand cDNA was synthesized using random hexamer primers followed by the second strand cDNA synthesis using either dUTP for directional library or dTTP for non directional library. For the non directional library it was ready post end repair A tailing adapter ligation size selection amplification and purification. For the directional library it was ready post end repair A tailing adapter ligation size selection USER enzyme digestion amplification and purification. The library was checked with Qubit and real time PCR for quantification and bioanalyzer for size distribution detection. Quantified libraries will be pooled and sequenced on Illumina platforms according to effective library concentration and data amount.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina HiSeq 4000", null, "SRP497581", null, "loader:fastq load.py", "WT_1_1.fq.gz WT_1_2.fq.gz", "fastq fastq", 6343747500.0, 21145825.0, "GSM8163701 r1", "0:150 1:150", "A:1783890425;C:1396753566;G:1403241010;T:1759774134;N:88365", 150, 150, null, null, 1783890425, 1396753566, 1403241010, 1759774134, 88365, "SRX24039365", "SRS20832130", "SRA1832826", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", "Bioinformatics, Max-Planck-Institute for Heart and Lung Research", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "random_priming", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-03-25", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31896, "SRR28745432", "SRX24311225", "SRS21073227", "SRP502845", "PRJNA1102356", "flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response", "GSE264406", "Transcriptome Analysis", "VEGFA administration has been explored as a pro angiogenic therapy for cardiovascular diseases including heart failure for several years; however many challenges remain. Here we investigate a different approach to augmenting VEGFA bioavailability one that achieves more physiological VEGFA concentrations by deleting VEGFR1/FLT1 a VEGFA decoy receptor. We find that following cryoinjury zebrafish flt1 mutant hearts display enhanced coronary revascularization and endocardial expansion increased cardiomyocyte dedifferentiation and proliferation and decreased scarring. Suppressing Vegfa signaling in flt1 mutants abrogates the beneficial effects of flt1 deletion. Transcriptomic analyses of cryoinjured flt1 mutant hearts revealed enhanced endothelial MAPK/ERK signaling and downregulation of the transcription factor gene egr3. Using genetic tools we observe egr3 upregulation in the regenerating endocardium and find that Egr3 promotes myofibroblast differentiation. These data suggest that with enhanced VEGFA bioavailability the cardiac endothelium limits myofibroblast differentiation via egr3 downregulation thereby providing a more permissive microenvironment for cardiomyocyte xxx post injury. Overall design: Comparative gene expression analysis between cryoinjured wild type zebrafish ventricles and flt1 mutant ventricles at 96 hours post cryoinjury.", null, "pubmed:39612288", null, "wild type heart 96 hours post cryoinjury 3", "GSM8217704", null, "source name:heart ventricle border z1 and injured area|tissue:heart ventricle border z1 and injured area|genotype:wild type|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing", "wild type heart 96 hours post cryoinjury 3", "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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 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. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: danRer11 Supplementary files format and content: library size normlized count matrix", "heart ventricle border zone and injured area", null, "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture\u2019s protocol Vazyme.", null, "tissue:heart ventricle border z1 and injured area|genotype:wild type|treatment:cardiac cryoinjury", "GSM8217704", "GSM8217704: wild type heart 96 hours post cryoinjury 3; Danio rerio; RNA Seq", "GSM8217704 r1", "GSM8217704", "1", "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture's protocol Vazyme.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP502845", null, "loader:fastq load.py", "E23_4173_Armaad_Lib_WT3_R1.fastq.gz", "fastq", 3257983192.0, 47556048.0, "GSM8217704 r1", "0:68.51", "A:848972796;C:741588101;G:760680137;T:905607069;N:1135089", 68, null, null, null, 848972796, 741588101, 760680137, 905607069, 1135089, "SRX24311225", "SRS21073227", "SRA1849558", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.94185, null, 0.087, null, 0.72478, null, 0.50388, null, 72, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-04-19", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31897, "SRR28745433", "SRX24311224", "SRS21073229", "SRP502845", "PRJNA1102356", "flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response", "GSE264406", "Transcriptome Analysis", "VEGFA administration has been explored as a pro angiogenic therapy for cardiovascular diseases including heart failure for several years; however many challenges remain. Here we investigate a different approach to augmenting VEGFA bioavailability one that achieves more physiological VEGFA concentrations by deleting VEGFR1/FLT1 a VEGFA decoy receptor. We find that following cryoinjury zebrafish flt1 mutant hearts display enhanced coronary revascularization and endocardial expansion increased cardiomyocyte dedifferentiation and proliferation and decreased scarring. Suppressing Vegfa signaling in flt1 mutants abrogates the beneficial effects of flt1 deletion. Transcriptomic analyses of cryoinjured flt1 mutant hearts revealed enhanced endothelial MAPK/ERK signaling and downregulation of the transcription factor gene egr3. Using genetic tools we observe egr3 upregulation in the regenerating endocardium and find that Egr3 promotes myofibroblast differentiation. These data suggest that with enhanced VEGFA bioavailability the cardiac endothelium limits myofibroblast differentiation via egr3 downregulation thereby providing a more permissive microenvironment for cardiomyocyte xxx post injury. Overall design: Comparative gene expression analysis between cryoinjured wild type zebrafish ventricles and flt1 mutant ventricles at 96 hours post cryoinjury.", null, "pubmed:39612288", null, "wild type heart 96 hours post cryoinjury 2", "GSM8217703", null, "source name:heart ventricle border z1 and injured area|tissue:heart ventricle border z1 and injured area|genotype:wild type|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing", "wild type heart 96 hours post cryoinjury 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 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. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: danRer11 Supplementary files format and content: library size normlized count matrix", "heart ventricle border zone and injured area", null, "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture\u2019s protocol Vazyme.", null, "tissue:heart ventricle border z1 and injured area|genotype:wild type|treatment:cardiac cryoinjury", "GSM8217703", "GSM8217703: wild type heart 96 hours post cryoinjury 2; Danio rerio; RNA Seq", "GSM8217703 r1", "GSM8217703", "1", "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture's protocol Vazyme.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP502845", null, "loader:fastq load.py", "E23_4173_Armaad_Lib_WT2_R1.fastq.gz", "fastq", 3864619254.0, 56519751.0, "GSM8217703 r1", "0:68.38", "A:1003402543;C:880721584;G:903469106;T:1075304136;N:1721885", 68, null, null, null, 1003402543, 880721584, 903469106, 1075304136, 1721885, "SRX24311224", "SRS21073229", "SRA1849558", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.93928, null, 0.08915, null, 0.72348, null, 0.49993, null, 71, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-04-19", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31898, "SRR28745434", "SRX24311223", "SRS21073228", "SRP502845", "PRJNA1102356", "flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response", "GSE264406", "Transcriptome Analysis", "VEGFA administration has been explored as a pro angiogenic therapy for cardiovascular diseases including heart failure for several years; however many challenges remain. Here we investigate a different approach to augmenting VEGFA bioavailability one that achieves more physiological VEGFA concentrations by deleting VEGFR1/FLT1 a VEGFA decoy receptor. We find that following cryoinjury zebrafish flt1 mutant hearts display enhanced coronary revascularization and endocardial expansion increased cardiomyocyte dedifferentiation and proliferation and decreased scarring. Suppressing Vegfa signaling in flt1 mutants abrogates the beneficial effects of flt1 deletion. Transcriptomic analyses of cryoinjured flt1 mutant hearts revealed enhanced endothelial MAPK/ERK signaling and downregulation of the transcription factor gene egr3. Using genetic tools we observe egr3 upregulation in the regenerating endocardium and find that Egr3 promotes myofibroblast differentiation. These data suggest that with enhanced VEGFA bioavailability the cardiac endothelium limits myofibroblast differentiation via egr3 downregulation thereby providing a more permissive microenvironment for cardiomyocyte xxx post injury. Overall design: Comparative gene expression analysis between cryoinjured wild type zebrafish ventricles and flt1 mutant ventricles at 96 hours post cryoinjury.", null, "pubmed:39612288", null, "wild type heart 96 hours post cryoinjury 1", "GSM8217702", null, "source name:heart ventricle border z1 and injured area|tissue:heart ventricle border z1 and injured area|genotype:wild type|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing", "wild type heart 96 hours post cryoinjury 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 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. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: danRer11 Supplementary files format and content: library size normlized count matrix", "heart ventricle border zone and injured area", null, "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture\u2019s protocol Vazyme.", null, "tissue:heart ventricle border z1 and injured area|genotype:wild type|treatment:cardiac cryoinjury", "GSM8217702", "GSM8217702: wild type heart 96 hours post cryoinjury 1; Danio rerio; RNA Seq", "GSM8217702 r1", "GSM8217702", "1", "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture's protocol Vazyme.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP502845", null, "loader:fastq load.py", "E23_4173_Armaad_Lib_WT1_R1.fastq.gz", "fastq", 3571478400.0, 52133215.0, "GSM8217702 r1", "0:68.51", "A:928171678;C:814216251;G:835024543;T:992630615;N:1435313", 68, null, null, null, 928171678, 814216251, 835024543, 992630615, 1435313, "SRX24311223", "SRS21073228", "SRA1849558", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.94111, null, 0.08647, null, 0.72922, null, 0.50812, null, 42, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-04-19", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31899, "SRR28745435", "SRX24311222", "SRS21073226", "SRP502845", "PRJNA1102356", "flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response", "GSE264406", "Transcriptome Analysis", "VEGFA administration has been explored as a pro angiogenic therapy for cardiovascular diseases including heart failure for several years; however many challenges remain. Here we investigate a different approach to augmenting VEGFA bioavailability one that achieves more physiological VEGFA concentrations by deleting VEGFR1/FLT1 a VEGFA decoy receptor. We find that following cryoinjury zebrafish flt1 mutant hearts display enhanced coronary revascularization and endocardial expansion increased cardiomyocyte dedifferentiation and proliferation and decreased scarring. Suppressing Vegfa signaling in flt1 mutants abrogates the beneficial effects of flt1 deletion. Transcriptomic analyses of cryoinjured flt1 mutant hearts revealed enhanced endothelial MAPK/ERK signaling and downregulation of the transcription factor gene egr3. Using genetic tools we observe egr3 upregulation in the regenerating endocardium and find that Egr3 promotes myofibroblast differentiation. These data suggest that with enhanced VEGFA bioavailability the cardiac endothelium limits myofibroblast differentiation via egr3 downregulation thereby providing a more permissive microenvironment for cardiomyocyte xxx post injury. Overall design: Comparative gene expression analysis between cryoinjured wild type zebrafish ventricles and flt1 mutant ventricles at 96 hours post cryoinjury.", null, "pubmed:39612288", null, "flt1 mutant heart 96 hours post cryoinjury 3", "GSM8217701", null, "source name:heart ventricle border z1 and injured area|tissue:heart ventricle border z1 and injured area|genotype:flt1bns29/bns29|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing", "flt1 mutant heart 96 hours post cryoinjury 3", "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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 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. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: danRer11 Supplementary files format and content: library size normlized count matrix", "heart ventricle border zone and injured area", null, "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture\u2019s protocol Vazyme.", null, "tissue:heart ventricle border z1 and injured area|genotype:flt1bns29/bns29|treatment:cardiac cryoinjury", "GSM8217701", "GSM8217701: flt1 mutant heart 96 hours post cryoinjury 3; Danio rerio; RNA Seq", "GSM8217701 r1", "GSM8217701", "1", "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture's protocol Vazyme.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP502845", null, "loader:fastq load.py", "E23_4173_Armaad_Lib_FLT_MUT3_R1.fastq.gz", "fastq", 4085359270.0, 59673604.0, "GSM8217701 r1", "0:68.46", "A:1050667797;C:938174838;G:953989485;T:1140941596;N:1585554", 68, null, null, null, 1050667797, 938174838, 953989485, 1140941596, 1585554, "SRX24311222", "SRS21073226", "SRA1849558", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.94035, null, 0.08631, null, 0.72376, null, 0.49828, null, 69, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-04-19", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31900, "SRR28745436", "SRX24311221", "SRS21073225", "SRP502845", "PRJNA1102356", "flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response", "GSE264406", "Transcriptome Analysis", "VEGFA administration has been explored as a pro angiogenic therapy for cardiovascular diseases including heart failure for several years; however many challenges remain. Here we investigate a different approach to augmenting VEGFA bioavailability one that achieves more physiological VEGFA concentrations by deleting VEGFR1/FLT1 a VEGFA decoy receptor. We find that following cryoinjury zebrafish flt1 mutant hearts display enhanced coronary revascularization and endocardial expansion increased cardiomyocyte dedifferentiation and proliferation and decreased scarring. Suppressing Vegfa signaling in flt1 mutants abrogates the beneficial effects of flt1 deletion. Transcriptomic analyses of cryoinjured flt1 mutant hearts revealed enhanced endothelial MAPK/ERK signaling and downregulation of the transcription factor gene egr3. Using genetic tools we observe egr3 upregulation in the regenerating endocardium and find that Egr3 promotes myofibroblast differentiation. These data suggest that with enhanced VEGFA bioavailability the cardiac endothelium limits myofibroblast differentiation via egr3 downregulation thereby providing a more permissive microenvironment for cardiomyocyte xxx post injury. Overall design: Comparative gene expression analysis between cryoinjured wild type zebrafish ventricles and flt1 mutant ventricles at 96 hours post cryoinjury.", null, "pubmed:39612288", null, "flt1 mutant heart 96 hours post cryoinjury 2", "GSM8217700", null, "source name:heart ventricle border z1 and injured area|tissue:heart ventricle border z1 and injured area|genotype:flt1bns29/bns29|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing", "flt1 mutant heart 96 hours post cryoinjury 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 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. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: danRer11 Supplementary files format and content: library size normlized count matrix", "heart ventricle border zone and injured area", null, "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture\u2019s protocol Vazyme.", null, "tissue:heart ventricle border z1 and injured area|genotype:flt1bns29/bns29|treatment:cardiac cryoinjury", "GSM8217700", "GSM8217700: flt1 mutant heart 96 hours post cryoinjury 2; Danio rerio; RNA Seq", "GSM8217700 r1", "GSM8217700", "1", "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture's protocol Vazyme.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP502845", null, "loader:fastq load.py", "E23_4173_Armaad_Lib_FLT_MUT2_R1.fastq.gz", "fastq", 4696922408.0, 68645737.0, "GSM8217700 r1", "0:68.42", "A:1220019708;C:1072448104;G:1106194472;T:1296618556;N:1641568", 68, null, null, null, 1220019708, 1072448104, 1106194472, 1296618556, 1641568, "SRX24311221", "SRS21073225", "SRA1849558", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.94205, null, 0.08792, null, 0.72543, null, 0.50566, null, 72, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-04-19", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [31901, "SRR28745437", "SRX24311220", "SRS21073224", "SRP502845", "PRJNA1102356", "flt1 inactivation promotes zebrafish cardiac regeneration by enhancing endothelial activity and limiting the fibrotic response", "GSE264406", "Transcriptome Analysis", "VEGFA administration has been explored as a pro angiogenic therapy for cardiovascular diseases including heart failure for several years; however many challenges remain. Here we investigate a different approach to augmenting VEGFA bioavailability one that achieves more physiological VEGFA concentrations by deleting VEGFR1/FLT1 a VEGFA decoy receptor. We find that following cryoinjury zebrafish flt1 mutant hearts display enhanced coronary revascularization and endocardial expansion increased cardiomyocyte dedifferentiation and proliferation and decreased scarring. Suppressing Vegfa signaling in flt1 mutants abrogates the beneficial effects of flt1 deletion. Transcriptomic analyses of cryoinjured flt1 mutant hearts revealed enhanced endothelial MAPK/ERK signaling and downregulation of the transcription factor gene egr3. Using genetic tools we observe egr3 upregulation in the regenerating endocardium and find that Egr3 promotes myofibroblast differentiation. These data suggest that with enhanced VEGFA bioavailability the cardiac endothelium limits myofibroblast differentiation via egr3 downregulation thereby providing a more permissive microenvironment for cardiomyocyte xxx post injury. Overall design: Comparative gene expression analysis between cryoinjured wild type zebrafish ventricles and flt1 mutant ventricles at 96 hours post cryoinjury.", null, "pubmed:39612288", null, "flt1 mutant heart 96 hours post cryoinjury 1", "GSM8217699", null, "source name:heart ventricle border z1 and injured area|tissue:heart ventricle border z1 and injured area|genotype:flt1bns29/bns29|treatment:cardiac cryoinjury|geo loc name:missing|collection date:missing", "flt1 mutant heart 96 hours post cryoinjury 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 Bolger et al. Trimmomatic: a flexible trimmer for Illumina sequence data. Reads were aligned versus Ensembl zebrafish genome version danRer11 Ensembl release 104 with STAR 2.7.10a Aligned reads were filtered to remove: duplicates with Picard 3.0.0 Picard: A set of tools in Java for working with next generation sequencing data in the BAM format multi mapping ribosomal or mitochondrial reads. Gene counts were established with featureCounts 2.0.4 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 raw count matrix was normalized with DESeq2 version 1.36.0 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. The Ensemble annotation was enriched with UniProt data Activities at the Universal Protein Resource UniProt. Assembly: danRer11 Supplementary files format and content: library size normlized count matrix", "heart ventricle border zone and injured area", null, "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture\u2019s protocol Vazyme.", null, "tissue:heart ventricle border z1 and injured area|genotype:flt1bns29/bns29|treatment:cardiac cryoinjury", "GSM8217699", "GSM8217699: flt1 mutant heart 96 hours post cryoinjury 1; Danio rerio; RNA Seq", "GSM8217699 r1", "GSM8217699", "1", "A pool of 5 ventricles was used per biological replicate. Total RNA was isolated using the miRNeasy micro Kit Qiagen combined with on column DNase digestion RNase Free DNase Set Qiagen 4\u00b5g of total RNA was used as input for VAHTS Stranded mRNA seq V6 Library preparation following manufacture's protocol Vazyme.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "SINGLE", "ILLUMINA", "NextSeq 2000", null, "SRP502845", null, "loader:fastq load.py", "E23_4173_Armaad_Lib_FLT_MUT1_R1.fastq.gz", "fastq", 2897934017.0, 42657803.0, "GSM8217699 r1", "0:67.93", "A:749045495;C:662930035;G:683478060;T:800853726;N:1626701", 67, null, null, null, 749045495, 662930035, 683478060, 800853726, 1626701, "SRX24311220", "SRS21073224", "SRA1849558", "MPI for heart and lung research", "MPI for heart and lung research", 1, 0.94107, null, 0.08304, null, 0.72579, null, 0.50482, null, 72, null, "B", null, "usable mapping rate", "illumina", "nextseq_v2", "unknown", "cdna_unspecified", "unknown", "bulk", "unknown", "unknown", null, "Germany", "2024-04-19", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 21 dpi sample 2", "GSM8506783", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2079206538, 1754420100, 1752583773, 2055108610, 59579, "SRX26043972", "SRS22614948", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 21 dpi sample 1", "GSM8506782", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2358947065, 1986782909, 1985349061, 2332333991, 67374, "SRX26043971", "SRS22614947", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 7 dpi sample 2", "GSM8506781", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2273220495, 1952762066, 1928310101, 2259829448, 121144, "SRX26043970", "SRS22614946", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 7 dpi sample 1", "GSM8506780", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1633289750, 1403959505, 1385683308, 1624058844, 83939, "SRX26043969", "SRS22614945", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 2 dpi sample 2", "GSM8506779", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1751063874, 1515880337, 1494689364, 1739782712, 91353, "SRX26043968", "SRS22614944", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 2 dpi sample 1", "GSM8506778", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1717644272, 1482451492, 1461128189, 1706373727, 90256, "SRX26043967", "SRS22614943", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 0 dpi sample 2", "GSM8506777", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2893792627, 2407838089, 2396125046, 2860411622, 81816, "SRX26043966", "SRS22614942", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "wild type 0 dpi sample 1", "GSM8506776", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2980386716, 2504687323, 2500279931, 2946028049, 84581, "SRX26043965", "SRS22614941", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 21 dpi sample 2", "GSM8506775", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2204157080, 1856260728, 1849823127, 2179439591, 63074, "SRX26043964", "SRS22614940", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 21 dpi sample 1", "GSM8506774", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2258410899, 1890202189, 1886482508, 2233018477, 63827, "SRX26043963", "SRS22614939", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 7 dpi sample 2", "GSM8506773", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1483061100, 1285068800, 1269689220, 1474711048, 70703, "SRX26043962", "SRS22614938", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 7 dpi sample 1", "GSM8506772", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1831140932, 1575183518, 1554676178, 1819734347, 96500, "SRX26043961", "SRS22614937", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 2 dpi sample 2", "GSM8506771", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1739648368, 1527224071, 1508002505, 1728567175, 89678, "SRX26043960", "SRS22614936", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 2 dpi sample 1", "GSM8506770", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 1522889953, 1312356884, 1296118643, 1514035483, 75875, "SRX26043959", "SRS22614935", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 0 dpi sample 2", "GSM8506769", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2514442400, 2095585016, 2092520078, 2482011445, 71861, "SRX26043958", "SRS22614934", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [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.", null, null, null, "nr4a1 mutant 0 dpi sample 1", "GSM8506768", null, "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", null, "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.", null, "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.", null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq X Plus", null, "SRP531880", null, null, "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, null, null, 2540516970, 2120755706, 2115163242, 2513633143, 71739, "SRX26043957", "SRS22614933", "SRA1968119", "The University of North Carolina", "The University of North Carolina", null, null, null, null, null, null, null, null, null, null, null, "B", "B", "biological fallback assumption", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "bulk", "bulk", "bulk", null, "United States", "2024-09-10", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34072, "SRR31040127", "SRX26425404", "SRS22944868", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited UI L004", "GSM8581895", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "Cited UI L004", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart", "GSM8581895", "GSM8581895: Cited UI L004; Danio rerio; RNA Seq", "GSM8581895 r1", "GSM8581895", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L004 R1 001.fastq.gz read2PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L004 R2 001.fastq.gz read3PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L004 I1 001.fastq.gz read4PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L004 I2 001.fastq.gz", "pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L004_I1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L004_I2_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L004_R1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L004_R2_001.fastq.gz", "fastq fastq fastq fastq", 8751034986.0, 63413297.0, "GSM8581895 r1", "0:28 1:90 2:10 3:10", "A:1848966031;C:1012706988;G:1157260676;T:1688231038;N:31997", 28, 90, 10, 10, 1848966031, 1012706988, 1157260676, 1688231038, 31997, "SRX26425404", "SRS22944868", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34073, "SRR31040128", "SRX26425403", "SRS22944867", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited UI L003", "GSM8581894", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "Cited UI L003", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart", "GSM8581894", "GSM8581894: Cited UI L003; Danio rerio; RNA Seq", "GSM8581894 r1", "GSM8581894", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L003 R1 001.fastq.gz read2PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L003 R2 001.fastq.gz read3PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L003 I1 001.fastq.gz read4PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L003 I2 001.fastq.gz", "pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L003_I1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L003_I2_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L003_R1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L003_R2_001.fastq.gz", "fastq fastq fastq fastq", 8965044420.0, 64964090.0, "GSM8581894 r1", "0:28 1:90 2:10 3:10", "A:1889187704;C:1042838950;G:1192357586;T:1722353910;N:29950", 28, 90, 10, 10, 1889187704, 1042838950, 1192357586, 1722353910, 29950, "SRX26425403", "SRS22944867", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34074, "SRR31040129", "SRX26425402", "SRS22944866", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited UI L002", "GSM8581893", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "Cited UI L002", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart", "GSM8581893", "GSM8581893: Cited UI L002; Danio rerio; RNA Seq", "GSM8581893 r1", "GSM8581893", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L002 R1 001.fastq.gz read2PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L002 R2 001.fastq.gz read3PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L002 I1 001.fastq.gz read4PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L002 I2 001.fastq.gz", "pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L002_I1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L002_I2_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L002_R1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L002_R2_001.fastq.gz", "fastq fastq fastq fastq", 9234521850.0, 66916825.0, "GSM8581893 r1", "0:28 1:90 2:10 3:10", "A:1942032508;C:1074923961;G:1229240783;T:1776284178;N:32820", 28, 90, 10, 10, 1942032508, 1074923961, 1229240783, 1776284178, 32820, "SRX26425402", "SRS22944866", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34075, "SRR31040130", "SRX26425401", "SRS22944865", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited UI L001", "GSM8581892", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "Cited UI L001", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:Uninjured heart", "GSM8581892", "GSM8581892: Cited UI L001; Danio rerio; RNA Seq", "GSM8581892 r1", "GSM8581892", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L001 R1 001.fastq.gz read2PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L001 R2 001.fastq.gz read3PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L001 I1 001.fastq.gz read4PairFiles=pt38a UI 022323 Tsang GEX LAF4954A26 S11 L001 I2 001.fastq.gz", "pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L001_I1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L001_I2_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L001_R1_001.fastq.gz pt38a_UI_022323_Tsang_GEX_LAF4954A26_S11_L001_R2_001.fastq.gz", "fastq fastq fastq fastq", 9307917288.0, 67448676.0, "GSM8581892 r1", "0:28 1:90 2:10 3:10", "A:1956920944;C:1083084138;G:1238610324;T:1791739835;N:25599", 28, 90, 10, 10, 1956920944, 1083084138, 1238610324, 1791739835, 25599, "SRX26425401", "SRS22944865", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34076, "SRR31040131", "SRX26425400", "SRS22944864", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited 3dpa L004", "GSM8581891", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "Cited 3dpa L004", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation", "GSM8581891", "GSM8581891: Cited 3dpa L004; Danio rerio; RNA Seq", "GSM8581891 r1", "GSM8581891", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L004 R1 001.fastq.gz read2PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L004 R2 001.fastq.gz read3PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L004 I1 001.fastq.gz read4PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L004 I2 001.fastq.gz", "pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L004_I1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L004_I2_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L004_R1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L004_R2_001.fastq.gz", "fastq fastq fastq fastq", 7170951684.0, 51963418.0, "GSM8581891 r1", "0:28 1:90 2:10 3:10", "A:1540735099;C:805699399;G:919379467;T:1410866922;N:26733", 28, 90, 10, 10, 1540735099, 805699399, 919379467, 1410866922, 26733, "SRX26425400", "SRS22944864", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34077, "SRR31040132", "SRX26425399", "SRS22944863", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited 3dpa L003", "GSM8581890", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "Cited 3dpa L003", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation", "GSM8581890", "GSM8581890: Cited 3dpa L003; Danio rerio; RNA Seq", "GSM8581890 r1", "GSM8581890", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L003 R1 001.fastq.gz read2PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L003 R2 001.fastq.gz read3PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L003 I1 001.fastq.gz read4PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L003 I2 001.fastq.gz", "pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L003_I1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L003_I2_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L003_R1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L003_R2_001.fastq.gz", "fastq fastq fastq fastq", 7291420716.0, 52836382.0, "GSM8581890 r1", "0:28 1:90 2:10 3:10", "A:1561481957;C:822744414;G:938546253;T:1432477210;N:24546", 28, 90, 10, 10, 1561481957, 822744414, 938546253, 1432477210, 24546, "SRX26425399", "SRS22944863", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34078, "SRR31040133", "SRX26425398", "SRS22944862", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited 3dpa L002", "GSM8581889", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "Cited 3dpa L002", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation", "GSM8581889", "GSM8581889: Cited 3dpa L002; Danio rerio; RNA Seq", "GSM8581889 r1", "GSM8581889", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L002 R1 001.fastq.gz read2PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L002 R2 001.fastq.gz read3PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L002 I1 001.fastq.gz read4PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L002 I2 001.fastq.gz", "pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L002_I1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L002_I2_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L002_R1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L002_R2_001.fastq.gz", "fastq fastq fastq fastq", 7477578162.0, 54185349.0, "GSM8581889 r1", "0:28 1:90 2:10 3:10", "A:1599788142;C:843874544;G:963283854;T:1469708656;N:26214", 28, 90, 10, 10, 1599788142, 843874544, 963283854, 1469708656, 26214, "SRX26425398", "SRS22944862", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34079, "SRR31040134", "SRX26425397", "SRS22944861", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "Cited 3dpa L001", "GSM8581888", null, "source name:heart|tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "Cited 3dpa L001", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:pt38a/pt38a|treatment:3 dy post amputation", "GSM8581888", "GSM8581888: Cited 3dpa L001; Danio rerio; RNA Seq", "GSM8581888 r1", "GSM8581888", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L001 R1 001.fastq.gz read2PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L001 R2 001.fastq.gz read3PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L001 I1 001.fastq.gz read4PairFiles=pt38a 3dpa 022323 Tsang GEX LAF4954A25 S4 L001 I2 001.fastq.gz", "pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L001_I1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L001_I2_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L001_R1_001.fastq.gz pt38a_3dpa_022323_Tsang_GEX_LAF4954A25_S4_L001_R2_001.fastq.gz", "fastq fastq fastq fastq", 7511701146.0, 54432617.0, "GSM8581888 r1", "0:28 1:90 2:10 3:10", "A:1606850913;C:847555151;G:967521409;T:1476987489;N:20568", 28, 90, 10, 10, 1606850913, 847555151, 967521409, 1476987489, 20568, "SRX26425397", "SRS22944861", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34080, "SRR31040135", "SRX26425396", "SRS22944860", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT UI L004", "GSM8581887", null, "source name:heart|tissue:heart|genotype:WT|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "WT UI L004", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:Uninjured heart", "GSM8581887", "GSM8581887: WT UI L004; Danio rerio; RNA Seq", "GSM8581887 r1", "GSM8581887", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L004 R1 001.fastq.gz read2PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L004 R2 001.fastq.gz read3PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L004 I1 001.fastq.gz read4PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L004 I2 001.fastq.gz", "WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L004_I1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L004_I2_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L004_R1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L004_R2_001.fastq.gz", "fastq fastq fastq fastq", 8744622816.0, 63366832.0, "GSM8581887 r1", "0:28 1:90 2:10 3:10", "A:1804235390;C:1112990195;G:1270205014;T:1515005620;N:578661", 28, 90, 10, 10, 1804235390, 1112990195, 1270205014, 1515005620, 578661, "SRX26425396", "SRS22944860", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34081, "SRR31040136", "SRX26425395", "SRS22944859", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT UI L003", "GSM8581886", null, "source name:heart|tissue:heart|genotype:WT|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "WT UI L003", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:Uninjured heart", "GSM8581886", "GSM8581886: WT UI L003; Danio rerio; RNA Seq", "GSM8581886 r1", "GSM8581886", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L003 R1 001.fastq.gz read2PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L003 R2 001.fastq.gz read3PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L003 I1 001.fastq.gz read4PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L003 I2 001.fastq.gz", "WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L003_I1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L003_I2_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L003_R1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L003_R2_001.fastq.gz", "fastq fastq fastq fastq", 8629549722.0, 62532969.0, "GSM8581886 r1", "0:28 1:90 2:10 3:10", "A:1780671193;C:1097605584;G:1253098096;T:1495999781;N:592556", 28, 90, 10, 10, 1780671193, 1097605584, 1253098096, 1495999781, 592556, "SRX26425395", "SRS22944859", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34082, "SRR31040137", "SRX26425394", "SRS22944858", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT UI L002", "GSM8581885", null, "source name:heart|tissue:heart|genotype:WT|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "WT UI L002", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:Uninjured heart", "GSM8581885", "GSM8581885: WT UI L002; Danio rerio; RNA Seq", "GSM8581885 r1", "GSM8581885", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L002 R1 001.fastq.gz read2PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L002 R2 001.fastq.gz read3PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L002 I1 001.fastq.gz read4PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L002 I2 001.fastq.gz", "WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L002_I1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L002_I2_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L002_R1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L002_R2_001.fastq.gz", "fastq fastq fastq fastq", 8810036748.0, 63840846.0, "GSM8581885 r1", "0:28 1:90 2:10 3:10", "A:1816298911;C:1122594552;G:1280394245;T:1525799551;N:588881", 28, 90, 10, 10, 1816298911, 1122594552, 1280394245, 1525799551, 588881, "SRX26425394", "SRS22944858", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34083, "SRR31040138", "SRX26425393", "SRS22944857", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT UI L001", "GSM8581884", null, "source name:heart|tissue:heart|genotype:WT|treatment:Uninjured heart|geo loc name:missing|collection date:missing", "WT UI L001", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:Uninjured heart", "GSM8581884", "GSM8581884: WT UI L001; Danio rerio; RNA Seq", "GSM8581884 r1", "GSM8581884", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L001 R1 001.fastq.gz read2PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L001 R2 001.fastq.gz read3PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L001 I1 001.fastq.gz read4PairFiles=WTVI 101222 Tsang Multiome GEX LAF3807A40 S24 L001 I2 001.fastq.gz", "WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L001_I1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L001_I2_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L001_R1_001.fastq.gz WTVI_101222_Tsang_Multiome_GEX_LAF3807A40_S24_L001_R2_001.fastq.gz", "fastq fastq fastq fastq", 8890601838.0, 64424651.0, "GSM8581884 r1", "0:28 1:90 2:10 3:10", "A:1831803855;C:1133337909;G:1293064278;T:1539489836;N:522712", 28, 90, 10, 10, 1831803855, 1133337909, 1293064278, 1539489836, 522712, "SRX26425393", "SRS22944857", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34084, "SRR31040139", "SRX26425392", "SRS22944856", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT 3dpa L004", "GSM8581883", null, "source name:heart|tissue:heart|genotype:WT|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "WT 3dpa L004", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:3 dy post amputation", "GSM8581883", "GSM8581883: WT 3dpa L004; Danio rerio; RNA Seq", "GSM8581883 r1", "GSM8581883", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L004 R1 001.fastq.gz read2PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L004 R2 001.fastq.gz read3PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L004 I1 001.fastq.gz read4PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L004 I2 001.fastq.gz", "WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L004_I1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L004_I2_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L004_R1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L004_R2_001.fastq.gz", "fastq fastq fastq fastq", 10259680380.0, 74345510.0, "GSM8581883 r1", "0:28 1:90 2:10 3:10", "A:2030501498;C:1372342288;G:1610608028;T:1676971327;N:672759", 28, 90, 10, 10, 2030501498, 1372342288, 1610608028, 1676971327, 672759, "SRX26425392", "SRS22944856", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34085, "SRR31040140", "SRX26425391", "SRS22944855", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT 3dpa L003", "GSM8581882", null, "source name:heart|tissue:heart|genotype:WT|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "WT 3dpa L003", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:3 dy post amputation", "GSM8581882", "GSM8581882: WT 3dpa L003; Danio rerio; RNA Seq", "GSM8581882 r1", "GSM8581882", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L003 R1 001.fastq.gz read2PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L003 R2 001.fastq.gz read3PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L003 I1 001.fastq.gz read4PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L003 I2 001.fastq.gz", "WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L003_I1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L003_I2_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L003_R1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L003_R2_001.fastq.gz", "fastq fastq fastq fastq", 10153022940.0, 73572630.0, "GSM8581882 r1", "0:28 1:90 2:10 3:10", "A:2010560616;C:1356907781;G:1592695197;T:1660694697;N:678409", 28, 90, 10, 10, 2010560616, 1356907781, 1592695197, 1660694697, 678409, "SRX26425391", "SRS22944855", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34086, "SRR31040141", "SRX26425390", "SRS22944854", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT 3dpa L002", "GSM8581881", null, "source name:heart|tissue:heart|genotype:WT|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "WT 3dpa L002", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:3 dy post amputation", "GSM8581881", "GSM8581881: WT 3dpa L002; Danio rerio; RNA Seq", "GSM8581881 r1", "GSM8581881", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L002 R1 001.fastq.gz read2PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L002 R2 001.fastq.gz read3PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L002 I1 001.fastq.gz read4PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L002 I2 001.fastq.gz", "WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L002_I1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L002_I2_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L002_R1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L002_R2_001.fastq.gz", "fastq fastq fastq fastq", 10374062784.0, 75174368.0, "GSM8581881 r1", "0:28 1:90 2:10 3:10", "A:2050663376;C:1389631407;G:1629809936;T:1694915558;N:672843", 28, 90, 10, 10, 2050663376, 1389631407, 1629809936, 1694915558, 672843, "SRX26425390", "SRS22944854", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34087, "SRR31040142", "SRX26425389", "SRS22944853", "SRP539406", "PRJNA1174776", "cited4a limits CM dedifferentiation and proliferation during zebrafish heart regeneration [snRNA seq]", "GSE279845", "Transcriptome Analysis", "Cardiac regeneration involves interplay of complex interactions between many different cell types including cardiomyocytes. The exact mechanism that enables cardiomyocytes to undergo dedifferentiation and proliferation to replace lost cells has been under intense study. Here we report single nuclear RNA sequencing profile of the injured zebrafish heart and identified distinct cardiomyocyte populations in the injured heart. These cardiomyocyte populations indicate diverse functions that includes stress response myofibril assembly proliferation and contraction. The contracting cardiomyocyte population also involves activation of maturation pathways as an early response to injury. This intriguing finding suggests that constant maintenance of distinctive terminally differentiated cardiomyocyte population is important for cardiac function during regeneration. To test this we determined that cited4a a p300/CBP transcriptional co activator is xxx post injury in mature cardiomyocyte population. Moreover loss of cited4a mutants showed increased dedifferentiation proliferation and accelerated heart regeneration. Thus suppressing cardiomyocyte maturation pathway activity in injured hearts could be an approach to promote heart regeneration. Overall design: Wildtype and cited4a mutant adult heart regeneration study injured by ventricular amputation. Hearts were collected at 3 dy post amputation dpa and uninjured controls UI. Extracted hearts were frozen in liquid Nitrogen and nuclei were isolated as described in methods section.", null, "pubmed:39713454", null, "WT 3dpa L001", "GSM8581880", null, "source name:heart|tissue:heart|genotype:WT|treatment:3 dy post amputation|geo loc name:missing|collection date:missing", "WT 3dpa L001", "Raw FASTQ files were processed and aligned using the Cell Ranger v. 7.0.0 \u201ccount\u201d utility with automatic chemistry detection aligning to the Danio reiro genome GRCz11.108. Processed counts were read into R v4.2.0 using the Seurat package v4.3.0. Nuclei were filtered for a minimum of 3 cells and 200 RNA features. Samples were filtered to exclude nuclei with abnormally high mitochondrial gene expression and RNA features to remove potential contamination and/or doublets. Assembly: GRCz11.108 Supplementary files format and content: matrix.mtx.gz Compressed filtered gene count matrix output by Cell Ranger for each cell in the respective sample. Supplementary files format and content: barcodes.tsv.gz Compressed filtered barcode table output by Cell Ranger with barcodes for each cell in the respective sample. Supplementary files format and content: features.tsv.gz Compressed feature table output by Cell Ranger with feature names for the ENSEMBL identifiers in the gene count matrix for the respective sample.", "heart", null, "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell 3\u2019 Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "tissue:heart|genotype:WT|treatment:3 dy post amputation", "GSM8581880", "GSM8581880: WT 3dpa L001; Danio rerio; RNA Seq", "GSM8581880 r1", "GSM8581880", "1", "Uninjured control hearts and 3 dy post amputation dpa were extracted washed in 1x PBS and and flash frozen in liquid Nitrogen. Nuclei were isolated as described in methods section using the Chromium Nuclei Isolation Kit with RNase Inhibitor PN 1000494. Library was constructed using the Chromium Next GEM Single Cell three prime Reagent Kits v3.1Dual Index according to the manufacturer's protocol and using the 10X Chromium Controller.", null, "RNA-Seq", "TRANSCRIPTOMIC SINGLE CELL", "cDNA", "PAIRED", "ILLUMINA", "Illumina NovaSeq 6000", null, "SRP539406", null, "loader:fastq load.py|options: readTypes=TBTT read1PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L001 R1 001.fastq.gz read2PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L001 R2 001.fastq.gz read3PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L001 I1 001.fastq.gz read4PairFiles=WT3dpa 101222 Tsang Multiome GEX LAF3807A41 S5 L001 I2 001.fastq.gz", "WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L001_I1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L001_I2_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L001_R1_001.fastq.gz WT3dpa_101222_Tsang_Multiome_GEX_LAF3807A41_S5_L001_R2_001.fastq.gz", "fastq fastq fastq fastq", 10577377770.0, 76647665.0, "GSM8581880 r1", "0:28 1:90 2:10 3:10", "A:2089361892;C:1417156705;G:1662751139;T:1728402830;N:617284", 28, 90, 10, 10, 2089361892, 1417156705, 1662751139, 1728402830, 617284, "SRX26425389", "SRS22944853", "SRA1993641", "Cell Biology, University of Pittsburgh", "Cell Biology, University of Pittsburgh", null, null, null, null, null, null, null, null, null, null, null, "B", null, "usable mapping rate", "illumina", "novaseq_era", "unknown", "cdna_unspecified", "unknown", "sc", "single_cell_droplet", "10x", null, "United States", "2024-10-18", "Undetermined", "Undetermined", "Heart", "Cardiovascular System"], [34987, "SRR32942209", "SRX28216558", "SRS24541720", "SRP573401", "PRJNA1233465", "An Organ wide Spatiotemporal Transcriptomic and Cellular Atlas of the Regenerating Zebrafish Heart", "PRJNA1233465", "Other", "Adult zebrafish robustly regenerate injured hearts through a complex orchestration of various cell types and a multitude of molecules. Here we utilize single cell RNA sequencing scRNA seq and Stereo seq to construct a spatially resolved cell dataset of regenerating zebrafish hearts across eight time points.", null, null, null, null, "spatial uninjured heart", null, "strain:not applicable|dev stage:uninjured|collection date:2021 08|geo loc name:China:Qingdao|sex:not applicable|tissue:heart|isolation source:spatial uninjured heart|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "Stereo seq of zebrafish heart", "DP8400023364BR L01 read.T1 C1.part 004", "DP8400023364BR L01 read.T1 C1.part 004", "Stereo seq of zebrafish heart", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "DNBSEQ", "DNBSEQ-T7", null, "SRP573401", null, null, "DP8400023364BR_L01_read.part_004_1.fq.gz DP8400023364BR_L01_read.part_004_2.fq.gz", "fastq fastq", 123077427480.0, 911684648.0, "DP8400023364BR L01 read.part 004 1.fq.gz", null, null, null, null, null, null, null, null, null, null, null, "SRX28216558", "SRS24541720", "SRA2105098", "BGI Research", "BGI Research Institute of Evolution and Marine Biodiversity, Ocean University of China", null, null, null, null, null, null, null, null, null, null, null, "T", "B", "mate1 technical by mapping diff", "bgi", "bgi", "unknown", "cdna_unspecified", "unknown", "sc_generic", "single_cell_generic", "generic-scrnaseq-only", null, "China", "2025-04-02", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [34988, "SRR32942163", "SRX28216557", "SRS24541723", "SRP573401", "PRJNA1233465", "An Organ wide Spatiotemporal Transcriptomic and Cellular Atlas of the Regenerating Zebrafish Heart", "PRJNA1233465", "Other", "Adult zebrafish robustly regenerate injured hearts through a complex orchestration of various cell types and a multitude of molecules. 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Here we utilize single cell RNA sequencing scRNA seq and Stereo seq to construct a spatially resolved cell dataset of regenerating zebrafish hearts across eight time points.", null, null, null, null, "spatial 3D heart", null, "strain:not applicable|dev stage:uninjured|collection date:2021 02|geo loc name:China:Qingdao|sex:not applicable|tissue:heart|isolation source:spatial 3D heart|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "Stereo seq of 3D zebrafish heart", "DP8400018806BL L01 read.DP8400016191TL D2.part 004", "DP8400018806BL L01 read.DP8400016191TL D2.part 004", "Stereo seq of 3D zebrafish heart", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "DNBSEQ", "DNBSEQ-T7", null, "SRP573401", null, null, "DP8400018806BL_L01_read.part_004_1.fq.gz DP8400018806BL_L01_read.part_004_2.fq.gz", "fastq fastq", 55082417580.0, 408017908.0, "DP8400018806BL L01 read.part 004 1.fq.gz", "0:35 1:100", "A:13778227671;C:14713292408;G:13807456331;T:12779522494;N:3918676", 35, 100, null, null, 13778227671, 14713292408, 13807456331, 12779522494, 3918676, "SRX28216555", "SRS24507277", "SRA2105098", "BGI Research", "BGI Research Institute of Evolution and Marine Biodiversity, Ocean University of China", null, null, null, null, null, null, null, null, null, null, null, "T", "T", "mates < 9% mapping rate", "bgi", "bgi", "unknown", "cdna_unspecified", "unknown", "sc_generic", "single_cell_generic", "generic-scrnaseq-only", null, "China", "2025-04-02", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [34991, "SRR32942166", "SRX28216554", "SRS24541719", "SRP573401", "PRJNA1233465", "An Organ wide Spatiotemporal Transcriptomic and Cellular Atlas of the Regenerating Zebrafish Heart", "PRJNA1233465", "Other", "Adult zebrafish robustly regenerate injured hearts through a complex orchestration of various cell types and a multitude of molecules. 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Here we utilize single cell RNA sequencing scRNA seq and Stereo seq to construct a spatially resolved cell dataset of regenerating zebrafish hearts across eight time points.", null, null, null, null, "spatial 3 dpa heart", null, "strain:not applicable|dev stage:3 dpa|collection date:2021 08|geo loc name:China:Qingdao|sex:not applicable|tissue:heart|isolation source:spatial 3 dpa heart|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "Stereo seq of zebrafish heart", "DP8400022389BL L01 read.T5 C2.part 004", "DP8400022389BL L01 read.T5 C2.part 004", "Stereo seq of zebrafish heart", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "cDNA", "PAIRED", "DNBSEQ", "DNBSEQ-T7", null, "SRP573401", null, null, "DP8400022389BL_L01_read.part_004_1.fq.gz DP8400022389BL_L01_read.part_004_2.fq.gz", "fastq fastq", 104447005335.0, 773681521.0, "DP8400022389BL L01 read.part 004 1.fq.gz", "0:35 1:100", "A:27343177960;C:27134625733;G:25518535252;T:24448625683;N:2040707", 35, 100, null, null, 27343177960, 27134625733, 25518535252, 24448625683, 2040707, "SRX28216553", "SRS24541721", "SRA2105098", "BGI Research", "BGI Research Institute of Evolution and Marine Biodiversity, Ocean University of China", null, null, null, null, null, null, null, null, null, null, null, "T", "B", "mate1 technical by mapping diff", "bgi", "bgi", "unknown", "cdna_unspecified", "unknown", "sc_generic", "single_cell_generic", "generic-scrnaseq-only", null, "China", "2025-04-02", "Undetermined", "Adult", "Heart", "Cardiovascular System"], [34993, "SRR32942168", "SRX28216552", "SRS24541722", "SRP573401", "PRJNA1233465", "An Organ wide Spatiotemporal Transcriptomic and Cellular Atlas of the Regenerating Zebrafish Heart", "PRJNA1233465", "Other", "Adult zebrafish robustly regenerate injured hearts through a complex orchestration of various cell types and a multitude of molecules. 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