{"database": "metadata", "table": "run_metadata", "is_view": false, "human_description_en": "where experiment.library_selection = \"size fractionation\", technology = \"unknown\" and tissue_curation_coarse = \"Cardiovascular System\"", "rows": [[37991, "SRR1265766", "SRX529160", "SRS598857", "SRP041544", "PRJNA245824", "Deep sequencing of small RNA facilitates tissue and sex associated microRNA discovery in zebrafish", "GSE57169", "Transcriptome Analysis", "The role of microRNAs in gene regulation has been well established. The extent of miRNA regulation also increases with increasing genome complexity. Though the number of genes appear to be equal between human and zebrafish substantially less microRNAs have been discovered in zebrafish compared to human Release 19. It appears that most of the miRNAs in zebrafish are yet to be discovered. We sequenced small RNAs from brain gut liver ovary testis eye heart and embryo of zebrafish. In brain gut and liver sequencing was done in male and female separately. Majority of the sequenced reads 16 62% mapped to known miRNAs with the exception of ovary 5.7% and testis 7.8%. Using the miRNA discovery tool miRDeep2 we discovered novel miRNAs from the un annotated reads that ranged from 7.6 to 23.0% with exceptions of ovary 51.4% and testis 55.2%. The prediction tool identified a total of 459 novel pre miRNAs. We compared expression of miRNAs between different tissues and between males and females to identify tissue associated and sex associated miRNAs respectively. These miRNAs could serve as putative biomarkers for these tissues. The brain and liver had highest number of tissue associated 22 and sex associated 34 miRNAs respectively. This study comprehensively identifies tissue and sex associated miRNAs in zebrafish. Further we have discovered 459 novel pre miRNAs 30% seed homology to human miRNA as a genomic resource which can facilitate further investigations to understand miRNA mRNA gene regulatory networks in zebrafish which will have implications in understanding the function of human homologs. Overall design: Known miRNA profiling novel miRNA discovery and identification of tissue associated and sex associated miRNAs from sRNA deep sequencing data of different tissues and embryo of zebrafish in triplicate was carried out using the Illumina HiSeq 2000 platform.", null, "pubmed:26574018", null, "Heart Replicate 3 sRNAseq", "GSM1376649", null, "source name:Heart|tissue:Heart|genetic background:Wild type Singapore strain", "Heart Replicate 3 sRNAseq", "Illumina Casava 1.8.2 software used for basecalling. The sequenced reads were first subjected to adapter removal through the cutadapt program Martin 2011. The trimmed reads were then collapsed to remove redundancy and to obtain a unique sequence fasta file through the mapper module of miRDeep2 package Friedl\u00e4nder et al. 2012. The unique reads fasta file was then put through an elimination pipeline module Vaz et al. 2010 comprising of a series of sequence similarity searches with the annotated databases. At each step the reads were matched to an annotated database with a maximum of two mismatches. The matched reads were removed and the unmatched ones were further matched to another annotated database finally culminating into an un annotated pool of reads that served as a source of novel miRNAs and novel sRNAs. The known miRNA expression profile was generated by using the quantifier module of the miRDeep2 package that gives the read counts for the known miRNAs. The quantifier.pl command line used: perl quantifier.pl p m r t Zebrafish The raw reads expression profile generated for all the replicates of the samples were subjected to Trimmed Mean of M values TMM normalisation using the Bioconductor package edgeR Robinson et al. 2010. Genome build: ZV9 Supplementary files format and content: 1. 'Danio rerio known miRNA Rel19 profile Raw.txt': Tab delimited text file that includes the raw counts for the known mature miRNA miRBase Release 19. Supplementary files format and content: 2. 'Danio rerio known miRNA Rel19 profile Normalised.txt': Tab delimited text file that includes the Trimmed Mean of M values TMM normalised counts for the known mature miRNA miRBase Release 19. One of the replicate of Heart MZH008 failed to cluster with the other two replicates on basis of its known miRNA expression profile and hence was not used for further analysis.", "Heart", "N/A", "Total RNA were extracted using mirVana\u2122 miRNA Isolation Kit AM1560 Life Technologies. Tissues were homogenised in 1.5 ml microfuge tube containing Lysis/Binding buffer provided in the mirVana\u2122 miRNA Isolation using a hand held pestle. Total RNA containing small RNA were purified following the manufacturer protocol. Small RNA libraries were prepared for sequencing using TruSeq Small RNA Sample Preparation Kit RS 200 0012 Illumina Inc.. Libraries were prepared according to manufacturer instructions. Briefly 1\u00b5g of good quality Total RNA per sample was used as starting material. 5\u2019 and 3\u2019 RNA adapters were ligated to each RNA molecule before reverse transcription to create single stranded cDNA. The cDNA was then amplified with PCR using a common primer and a primer containing a unique index sequence. The resulting PCR reactions were electrophoresed on 6% Novex TBE PAGE Gel Life Technologies and bands corresponding to adapter ligated constructs derived from 22 30 nucleotides small RNA fragments were excised from the gel. The small RNA were purified from the excised gel and validated on High Sensitivity DNA chips on a Bioanalyser Agilent Technologies before sequencing.", "Fishes were purchased from a local supplier and acclimatized before tissue extraction.", "tissue:Heart|genetic background:Wild type Singapore strain", "GSM1376649", "GSM1376649: Heart Replicate 3 sRNAseq; Danio rerio; miRNA Seq", "GSM1376649", null, "1", "Total RNA were extracted using mirVana\u2122 miRNA Isolation Kit AM1560 Life Technologies. Tissues were homogenised in 1.5 ml microfuge tube containing Lysis/Binding buffer provided in the mirVana\u2122 miRNA Isolation using a hand held pestle. Total RNA containing small RNA were purified following the manufacturer protocol. Small RNA libraries were prepared for sequencing using TruSeq Small RNA Sample Preparation Kit RS 200 0012 Illumina Inc.. Libraries were prepared according to manufacturer instructions. Briefly 1\u00b5g of good quality Total RNA per sample was used as starting material. 5\u2019 and 3\u2019 RNA adapters were ligated to each RNA molecule before reverse transcription to create single stranded cDNA. The cDNA was then amplified with PCR using a common primer and a primer containing a unique index sequence. The resulting PCR reactions were electrophoresed on 6% Novex TBE PAGE Gel Life Technologies and bands corresponding to adapter ligated constructs derived from 22 30 nucleotides small RNA fragments were excised from the gel. The small RNA were purified from the excised gel and validated on High Sensitivity DNA chips on a Bioanalyser Agilent Technologies before sequencing.", "GEO Accession:GSM1376649", "miRNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "SINGLE", "ILLUMINA", "Illumina HiSeq 2000", null, "SRP041544", null, null, "MZH008_GATCAG_L005_R1.fastq.gz", "fastq", 4401229692.0, 57910917.0, "GSM1376649 r1", "0:76", "A:1009381958;C:1130057881;G:1173217392;T:1088123982;N:448479", 76, null, null, null, 1009381958, 1130057881, 1173217392, 1088123982, 448479, "SRX529160", "SRS598857", "SRA160430", "GEO", "Expression and Signaling in Mesenchymal and Hematopoietic Stem Cells, Genome and Gene Expression Data Analysis Division, Bioinformatics Institute, A*STAR, Singapore", 1, 0.00129, null, 0.00046, null, 0.99882, null, 0.51351, null, 76, null, "T", null, "under 1.2% mapping rate", "illumina", "hiseq_era", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "Singapore", "2014-04-29", "Undetermined", "Embryo", "Heart", "Cardiovascular System"], [37992, "SRR1265765", "SRX529159", "SRS598856", "SRP041544", "PRJNA245824", "Deep sequencing of small RNA facilitates tissue and sex associated microRNA discovery in zebrafish", "GSE57169", "Transcriptome Analysis", "The role of microRNAs in gene regulation has been well established. The extent of miRNA regulation also increases with increasing genome complexity. Though the number of genes appear to be equal between human and zebrafish substantially less microRNAs have been discovered in zebrafish compared to human Release 19. It appears that most of the miRNAs in zebrafish are yet to be discovered. We sequenced small RNAs from brain gut liver ovary testis eye heart and embryo of zebrafish. In brain gut and liver sequencing was done in male and female separately. Majority of the sequenced reads 16 62% mapped to known miRNAs with the exception of ovary 5.7% and testis 7.8%. Using the miRNA discovery tool miRDeep2 we discovered novel miRNAs from the un annotated reads that ranged from 7.6 to 23.0% with exceptions of ovary 51.4% and testis 55.2%. The prediction tool identified a total of 459 novel pre miRNAs. We compared expression of miRNAs between different tissues and between males and females to identify tissue associated and sex associated miRNAs respectively. These miRNAs could serve as putative biomarkers for these tissues. The brain and liver had highest number of tissue associated 22 and sex associated 34 miRNAs respectively. This study comprehensively identifies tissue and sex associated miRNAs in zebrafish. Further we have discovered 459 novel pre miRNAs 30% seed homology to human miRNA as a genomic resource which can facilitate further investigations to understand miRNA mRNA gene regulatory networks in zebrafish which will have implications in understanding the function of human homologs. Overall design: Known miRNA profiling novel miRNA discovery and identification of tissue associated and sex associated miRNAs from sRNA deep sequencing data of different tissues and embryo of zebrafish in triplicate was carried out using the Illumina HiSeq 2000 platform.", null, "pubmed:26574018", null, "Heart Replicate 2 sRNAseq", "GSM1376648", null, "source name:Heart|tissue:Heart|genetic background:Wild type Singapore strain", "Heart Replicate 2 sRNAseq", "Illumina Casava 1.8.2 software used for basecalling. The sequenced reads were first subjected to adapter removal through the cutadapt program Martin 2011. The trimmed reads were then collapsed to remove redundancy and to obtain a unique sequence fasta file through the mapper module of miRDeep2 package Friedl\u00e4nder et al. 2012. The unique reads fasta file was then put through an elimination pipeline module Vaz et al. 2010 comprising of a series of sequence similarity searches with the annotated databases. At each step the reads were matched to an annotated database with a maximum of two mismatches. The matched reads were removed and the unmatched ones were further matched to another annotated database finally culminating into an un annotated pool of reads that served as a source of novel miRNAs and novel sRNAs. The known miRNA expression profile was generated by using the quantifier module of the miRDeep2 package that gives the read counts for the known miRNAs. The quantifier.pl command line used: perl quantifier.pl p m r t Zebrafish The raw reads expression profile generated for all the replicates of the samples were subjected to Trimmed Mean of M values TMM normalisation using the Bioconductor package edgeR Robinson et al. 2010. Genome build: ZV9 Supplementary files format and content: 1. 'Danio rerio known miRNA Rel19 profile Raw.txt': Tab delimited text file that includes the raw counts for the known mature miRNA miRBase Release 19. Supplementary files format and content: 2. 'Danio rerio known miRNA Rel19 profile Normalised.txt': Tab delimited text file that includes the Trimmed Mean of M values TMM normalised counts for the known mature miRNA miRBase Release 19. One of the replicate of Heart MZH008 failed to cluster with the other two replicates on basis of its known miRNA expression profile and hence was not used for further analysis.", "Heart", "N/A", "Total RNA were extracted using mirVana\u2122 miRNA Isolation Kit AM1560 Life Technologies. Tissues were homogenised in 1.5 ml microfuge tube containing Lysis/Binding buffer provided in the mirVana\u2122 miRNA Isolation using a hand held pestle. Total RNA containing small RNA were purified following the manufacturer protocol. Small RNA libraries were prepared for sequencing using TruSeq Small RNA Sample Preparation Kit RS 200 0012 Illumina Inc.. Libraries were prepared according to manufacturer instructions. Briefly 1\u00b5g of good quality Total RNA per sample was used as starting material. 5\u2019 and 3\u2019 RNA adapters were ligated to each RNA molecule before reverse transcription to create single stranded cDNA. The cDNA was then amplified with PCR using a common primer and a primer containing a unique index sequence. The resulting PCR reactions were electrophoresed on 6% Novex TBE PAGE Gel Life Technologies and bands corresponding to adapter ligated constructs derived from 22 30 nucleotides small RNA fragments were excised from the gel. The small RNA were purified from the excised gel and validated on High Sensitivity DNA chips on a Bioanalyser Agilent Technologies before sequencing.", "Fishes were purchased from a local supplier and acclimatized before tissue extraction.", "tissue:Heart|genetic background:Wild type Singapore strain", "GSM1376648", "GSM1376648: Heart Replicate 2 sRNAseq; Danio rerio; miRNA Seq", "GSM1376648", null, "1", "Total RNA were extracted using mirVana\u2122 miRNA Isolation Kit AM1560 Life Technologies. Tissues were homogenised in 1.5 ml microfuge tube containing Lysis/Binding buffer provided in the mirVana\u2122 miRNA Isolation using a hand held pestle. Total RNA containing small RNA were purified following the manufacturer protocol. Small RNA libraries were prepared for sequencing using TruSeq Small RNA Sample Preparation Kit RS 200 0012 Illumina Inc.. Libraries were prepared according to manufacturer instructions. Briefly 1\u00b5g of good quality Total RNA per sample was used as starting material. 5\u2019 and 3\u2019 RNA adapters were ligated to each RNA molecule before reverse transcription to create single stranded cDNA. The cDNA was then amplified with PCR using a common primer and a primer containing a unique index sequence. The resulting PCR reactions were electrophoresed on 6% Novex TBE PAGE Gel Life Technologies and bands corresponding to adapter ligated constructs derived from 22 30 nucleotides small RNA fragments were excised from the gel. The small RNA were purified from the excised gel and validated on High Sensitivity DNA chips on a Bioanalyser Agilent Technologies before sequencing.", "GEO Accession:GSM1376648", "miRNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "SINGLE", "ILLUMINA", "Illumina HiSeq 2000", null, "SRP041544", null, null, "MZH007_ACTTGA_L005_R1.fastq.gz", "fastq", 3202357508.0, 42136283.0, "GSM1376648 r1", "0:76", "A:666309720;C:845347679;G:846066601;T:844306103;N:327405", 76, null, null, null, 666309720, 845347679, 846066601, 844306103, 327405, "SRX529159", "SRS598856", "SRA160430", "GEO", "Expression and Signaling in Mesenchymal and Hematopoietic Stem Cells, Genome and Gene Expression Data Analysis Division, Bioinformatics Institute, A*STAR, Singapore", 1, 0.00042, null, 3e-05, null, 0.99924, null, 0.56521, null, 76, null, "T", null, "under 1.2% mapping rate", "illumina", "hiseq_era", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "Singapore", "2014-04-29", "Undetermined", "Embryo", "Heart", "Cardiovascular System"], [37993, "SRR1265764", "SRX529158", "SRS598855", "SRP041544", "PRJNA245824", "Deep sequencing of small RNA facilitates tissue and sex associated microRNA discovery in zebrafish", "GSE57169", "Transcriptome Analysis", "The role of microRNAs in gene regulation has been well established. The extent of miRNA regulation also increases with increasing genome complexity. Though the number of genes appear to be equal between human and zebrafish substantially less microRNAs have been discovered in zebrafish compared to human Release 19. It appears that most of the miRNAs in zebrafish are yet to be discovered. We sequenced small RNAs from brain gut liver ovary testis eye heart and embryo of zebrafish. In brain gut and liver sequencing was done in male and female separately. Majority of the sequenced reads 16 62% mapped to known miRNAs with the exception of ovary 5.7% and testis 7.8%. Using the miRNA discovery tool miRDeep2 we discovered novel miRNAs from the un annotated reads that ranged from 7.6 to 23.0% with exceptions of ovary 51.4% and testis 55.2%. The prediction tool identified a total of 459 novel pre miRNAs. We compared expression of miRNAs between different tissues and between males and females to identify tissue associated and sex associated miRNAs respectively. These miRNAs could serve as putative biomarkers for these tissues. The brain and liver had highest number of tissue associated 22 and sex associated 34 miRNAs respectively. This study comprehensively identifies tissue and sex associated miRNAs in zebrafish. Further we have discovered 459 novel pre miRNAs 30% seed homology to human miRNA as a genomic resource which can facilitate further investigations to understand miRNA mRNA gene regulatory networks in zebrafish which will have implications in understanding the function of human homologs. Overall design: Known miRNA profiling novel miRNA discovery and identification of tissue associated and sex associated miRNAs from sRNA deep sequencing data of different tissues and embryo of zebrafish in triplicate was carried out using the Illumina HiSeq 2000 platform.", null, "pubmed:26574018", null, "Heart Replicate 1 sRNAseq", "GSM1376647", null, "source name:Heart|tissue:Heart|genetic background:Wild type Singapore strain", "Heart Replicate 1 sRNAseq", "Illumina Casava 1.8.2 software used for basecalling. The sequenced reads were first subjected to adapter removal through the cutadapt program Martin 2011. The trimmed reads were then collapsed to remove redundancy and to obtain a unique sequence fasta file through the mapper module of miRDeep2 package Friedl\u00e4nder et al. 2012. The unique reads fasta file was then put through an elimination pipeline module Vaz et al. 2010 comprising of a series of sequence similarity searches with the annotated databases. At each step the reads were matched to an annotated database with a maximum of two mismatches. The matched reads were removed and the unmatched ones were further matched to another annotated database finally culminating into an un annotated pool of reads that served as a source of novel miRNAs and novel sRNAs. The known miRNA expression profile was generated by using the quantifier module of the miRDeep2 package that gives the read counts for the known miRNAs. The quantifier.pl command line used: perl quantifier.pl p m r t Zebrafish The raw reads expression profile generated for all the replicates of the samples were subjected to Trimmed Mean of M values TMM normalisation using the Bioconductor package edgeR Robinson et al. 2010. Genome build: ZV9 Supplementary files format and content: 1. 'Danio rerio known miRNA Rel19 profile Raw.txt': Tab delimited text file that includes the raw counts for the known mature miRNA miRBase Release 19. Supplementary files format and content: 2. 'Danio rerio known miRNA Rel19 profile Normalised.txt': Tab delimited text file that includes the Trimmed Mean of M values TMM normalised counts for the known mature miRNA miRBase Release 19. One of the replicate of Heart MZH008 failed to cluster with the other two replicates on basis of its known miRNA expression profile and hence was not used for further analysis.", "Heart", "N/A", "Total RNA were extracted using mirVana\u2122 miRNA Isolation Kit AM1560 Life Technologies. Tissues were homogenised in 1.5 ml microfuge tube containing Lysis/Binding buffer provided in the mirVana\u2122 miRNA Isolation using a hand held pestle. Total RNA containing small RNA were purified following the manufacturer protocol. Small RNA libraries were prepared for sequencing using TruSeq Small RNA Sample Preparation Kit RS 200 0012 Illumina Inc.. Libraries were prepared according to manufacturer instructions. Briefly 1\u00b5g of good quality Total RNA per sample was used as starting material. 5\u2019 and 3\u2019 RNA adapters were ligated to each RNA molecule before reverse transcription to create single stranded cDNA. The cDNA was then amplified with PCR using a common primer and a primer containing a unique index sequence. The resulting PCR reactions were electrophoresed on 6% Novex TBE PAGE Gel Life Technologies and bands corresponding to adapter ligated constructs derived from 22 30 nucleotides small RNA fragments were excised from the gel. The small RNA were purified from the excised gel and validated on High Sensitivity DNA chips on a Bioanalyser Agilent Technologies before sequencing.", "Fishes were purchased from a local supplier and acclimatized before tissue extraction.", "tissue:Heart|genetic background:Wild type Singapore strain", "GSM1376647", "GSM1376647: Heart Replicate 1 sRNAseq; Danio rerio; miRNA Seq", "GSM1376647", null, "1", "Total RNA were extracted using mirVana\u2122 miRNA Isolation Kit AM1560 Life Technologies. Tissues were homogenised in 1.5 ml microfuge tube containing Lysis/Binding buffer provided in the mirVana\u2122 miRNA Isolation using a hand held pestle. Total RNA containing small RNA were purified following the manufacturer protocol. Small RNA libraries were prepared for sequencing using TruSeq Small RNA Sample Preparation Kit RS 200 0012 Illumina Inc.. Libraries were prepared according to manufacturer instructions. Briefly 1\u00b5g of good quality Total RNA per sample was used as starting material. 5\u2019 and 3\u2019 RNA adapters were ligated to each RNA molecule before reverse transcription to create single stranded cDNA. The cDNA was then amplified with PCR using a common primer and a primer containing a unique index sequence. The resulting PCR reactions were electrophoresed on 6% Novex TBE PAGE Gel Life Technologies and bands corresponding to adapter ligated constructs derived from 22 30 nucleotides small RNA fragments were excised from the gel. The small RNA were purified from the excised gel and validated on High Sensitivity DNA chips on a Bioanalyser Agilent Technologies before sequencing.", "GEO Accession:GSM1376647", "miRNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "SINGLE", "ILLUMINA", "Illumina HiSeq 2000", null, "SRP041544", null, null, "MZH002_CAGATC_L005_R1.fastq.gz", "fastq", 3777814232.0, 49708082.0, "GSM1376647 r1", "0:76", "A:791204432;C:1050679958;G:1001897360;T:933655799;N:376683", 76, null, null, null, 791204432, 1050679958, 1001897360, 933655799, 376683, "SRX529158", "SRS598855", "SRA160430", "GEO", "Expression and Signaling in Mesenchymal and Hematopoietic Stem Cells, Genome and Gene Expression Data Analysis Division, Bioinformatics Institute, A*STAR, Singapore", 1, 0.00034, null, 4e-05, null, 0.99943, null, 0.62264, null, 76, null, "T", null, "under 1.2% mapping rate", "illumina", "hiseq_era", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "Singapore", "2014-04-29", "Undetermined", "Embryo", "Heart", "Cardiovascular System"], [40972, "SRR3498294", "SRX1756840", "SRS1433371", "SRP074848", "PRJNA321321", "microRNAs Establish and Maintain Uniform Cellular Phenotypes during the Architecture of Complex Tissues", "GSE81340", "Transcriptome Analysis", "Proper functioning of tissues requires cells to behave in uniform well organized ways. Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "NoEndo 72hpf E2", "GSM2150819", null, "source name:Endothelial cell|developmental stage:72hpf|tissue:Endothelial|stain:GFP", "NoEndo 72hpf E2", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. Illumina TruSeq RNA libraries were prepared for sequencing using standard Illumina protocols", "Zebrafish embryos were raised according standard protocols at 28\u02daC and according to protocols approved by Yale University Institutional Animal Care and Use Committee # 2015 11473.", "developmental stage:72hpf|tissue:Endothelial|stain:GFP", "GSM2150819", "GSM2150819: NoEndo 72hpf E2; Danio rerio; miRNA Seq", "GSM2150819", null, "1", "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. Illumina TruSeq RNA libraries were prepared for sequencing using standard Illumina protocols", "GEO Accession:GSM2150819", "miRNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "SINGLE", "ILLUMINA", "Illumina Genome Analyzer", null, "SRP074848", null, null, "NoEndo_72hpf_E2.fastq.gz", "fastq", 797509876.0, 10493551.0, "GSM2150819 r1", "0:76", "A:182564842;C:199547592;G:199064466;T:216287390;N:45586", 76, null, null, null, 182564842, 199547592, 199064466, 216287390, 45586, "SRX1756840", "SRS1433371", "SRA424808", "GEO", "Internal Medicine, Yale University", 1, 1e-05, null, 0.0, null, 1.0, null, null, null, 76, null, "T", null, "under 1.2% mapping rate", "illumina", "early_illumina", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "United States", "2016-05-11", "Larval", "Larval", "Endothelium", "Cardiovascular System"], [40973, "SRR3498293", "SRX1756839", "SRS1433370", "SRP074848", "PRJNA321321", "microRNAs Establish and Maintain Uniform Cellular Phenotypes during the Architecture of Complex Tissues", "GSE81340", "Transcriptome Analysis", "Proper functioning of tissues requires cells to behave in uniform well organized ways. Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "NoEndo 72hpf E1", "GSM2150818", null, "source name:Endothelial cell|developmental stage:72hpf|tissue:Endothelial|stain:GFP", "NoEndo 72hpf E1", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. Illumina TruSeq RNA libraries were prepared for sequencing using standard Illumina protocols", "Zebrafish embryos were raised according standard protocols at 28\u02daC and according to protocols approved by Yale University Institutional Animal Care and Use Committee # 2015 11473.", "developmental stage:72hpf|tissue:Endothelial|stain:GFP", "GSM2150818", "GSM2150818: NoEndo 72hpf E1; Danio rerio; miRNA Seq", "GSM2150818", null, "1", "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. Illumina TruSeq RNA libraries were prepared for sequencing using standard Illumina protocols", "GEO Accession:GSM2150818", "miRNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "SINGLE", "ILLUMINA", "Illumina Genome Analyzer", null, "SRP074848", null, null, "NoEndo_72hpf_E1.fastq.gz", "fastq", 1864172232.0, 24528582.0, "GSM2150818 r1", "0:76", "A:426671762;C:469538477;G:458132395;T:509711525;N:118073", 76, null, null, null, 426671762, 469538477, 458132395, 509711525, 118073, "SRX1756839", "SRS1433370", "SRA424808", "GEO", "Internal Medicine, Yale University", 1, 0.0, null, 0.0, null, 1.0, null, null, null, 76, null, "T", null, "under 1.2% mapping rate", "illumina", "early_illumina", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "United States", "2016-05-11", "Larval", "Larval", "Endothelium", "Cardiovascular System"], [40974, "SRR3498292", "SRX1756838", "SRS1433369", "SRP074848", "PRJNA321321", "microRNAs Establish and Maintain Uniform Cellular Phenotypes during the Architecture of Complex Tissues", "GSE81340", "Transcriptome Analysis", "Proper functioning of tissues requires cells to behave in uniform well organized ways. Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "NoEndo 6dpf E1", "GSM2150817", null, "source name:Endothelial cell|developmental stage:6dpf|tissue:Endothelial|stain:GFP", "NoEndo 6dpf E1", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "NoEndo 48hpf E2", "GSM2150816", null, "source name:Endothelial cell|developmental stage:48hpf|tissue:Endothelial|stain:GFP", "NoEndo 48hpf E2", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "NoEndo 48hpf E1", "GSM2150815", null, "source name:Endothelial cell|developmental stage:48hpf|tissue:Endothelial|stain:GFP", "NoEndo 48hpf E1", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "NoEndo 24hpf E1", "GSM2150814", null, "source name:Endothelial cell|developmental stage:24hpf|tissue:Endothelial|stain:GFP", "NoEndo 24hpf E1", "Illumina Casava1.7 software used for basecalling. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "Endo 72hpf E2", "GSM2150813", null, "source name:Endothelial cell|developmental stage:72hpf|tissue:Endothelial|stain:GFP", "Endo 72hpf E2", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "Endo 72hpf E1", "GSM2150812", null, "source name:Endothelial cell|developmental stage:72hpf|tissue:Endothelial|stain:GFP", "Endo 72hpf E1", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "Endo 6dpf E1", "GSM2150811", null, "source name:Endothelial cell|developmental stage:6dpf|tissue:Endothelial|stain:GFP", "Endo 6dpf E1", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "Endo 48hpf E2", "GSM2150810", null, "source name:Endothelial cell|developmental stage:48hpf|tissue:Endothelial|stain:GFP", "Endo 48hpf E2", "Illumina Casava1.7 software used for basecalling. Sequenced reads were trimmed for adaptor sequence and masked for low complexity or low quality sequence then mapped to Zv9 whole genome using STAR v2.3.0 Fragments Per Kilobase Of Exon Per Million Fragments Mapped FPKM were calculated using Cufflink software Annotation gtf for Zv9 Genome build: Zv9 Supplementary files format and content: tab delimited text files include RPKM values for each Sample ...", "Endothelial cell", null, "Transgenic fish were treated with Liberase to disociate the cells. post FACS sorting the GFP positive cells were lisate and RNA was harvested using Trizol reagent. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "Endo 48hpf E1", "GSM2150809", null, "source name:Endothelial cell|developmental stage:48hpf|tissue:Endothelial|stain:GFP", "Endo 48hpf E1", "Illumina Casava1.7 software used for basecalling. 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Conversely many diseases involve increased cellular heterogeneity due to genetic and epigenetic alterations. Defining the mechanisms that counteract phenotypic variability is therefore critical to understand how tissues sustain homeostasis. Here we carried out a single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single microRNA miRNA genes and multi gene miRNA families. We found that miRNA mutants exhibit a profound increase in cellular phenotypic variability of specific vascular traits. Genome wide analysis of endothelial miRNA target genes identified antagonistic regulatory nodes of vascular growth and morphogenesis signaling that allow variable cell behaviors when derepressed. Remarkably lack of such miRNA activity greatly sensitized the vascular system to microenvironmental changes induced by pharmacological stress. We uncover a previously unrecognized role of miRNAs as a widespread protective mechanism that limits variability in cellular phenotypes. This discovery marks an important advance in our comprehension of how miRNAs function in the physiology of higher organisms. Overall design: Analysis of differential genes expression in Zebrafish endothelial cells for 4 different developmental stages in duplicate", "parent bioproject:PRJNA321317", "pubmed:28350988;pubmed:33273096", null, "Endo 24hpf E1", "GSM2150808", null, "source name:Endothelial cell|developmental stage:24hpf|tissue:Endothelial|stain:GFP", "Endo 24hpf E1", "Illumina Casava1.7 software used for basecalling. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. Finally we examined the upregulation of repetitive elements in hemogenic endothelial cells post treatment with valproic acid VPA or decitabine.", null, null, null, null, "danRer10 raw data", null, "strain:AB/tu|age:not applicable|sex:pooled male and female|tissue:endothelial and hemogenic endothelial|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq rig 1 lgp2 morpholino injected endothelial hemogenic endothelial cell 26hpf replicate 2", "16", "16", "TruSeq stranded mRNA", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "PAIRED", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP226614", null, null, "RNA_seq rig_1_lgp2 morpholino injected endothelial_hemogenic endothelial cell 26hpf replicate 2_R2.fastq.gz RNA_seq rig_1_lgp2 morpholino injected endothelial_hemogenic endothelial cell 26hpf replicate 2_R1.fastq.gz", "fastq fastq", 2071385250.0, 13809235.0, "RNA seq rig 1 lgp2 morpholino injected endothelial hemogenic endothelial cell 26hpf replicate 2 R1.fastq.gz", "0:75 1:75", "A:497024628;C:535934066;G:538798491;T:499539772;N:88293", 75, 75, null, null, 497024628, 535934066, 538798491, 499539772, 88293, "SRX7034690", "SRS5554730", "SRA983011", "Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany|Department of Cellular and Molecular Immunology", "Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany", 2, 0.92507, 0.92563, 0.0745, 0.07106, 0.74148, 0.74186, 0.5137, 0.52923, 75, 75, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "Germany", "2019-10-24", "Pharyngula", "Embryo", "Endothelium", "Cardiovascular System"], [55396, "SRR10323908", "SRX7034689", "SRS5554730", "SRP226614", "PRJNA578896", "Repetitive elements engage Rig I and Mda5 in interplay with Lgp2 to enhance hematopoietic stem cell emergence", "PRJNA578896", "Other", "In this study we examine the role of RIG I like receptors RLRs in hematopoietic stem and progenitor cell formation. We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. Finally we examined the upregulation of repetitive elements in hemogenic endothelial cells post treatment with valproic acid VPA or decitabine.", null, null, null, null, "danRer10 raw data", null, "strain:AB/tu|age:not applicable|sex:pooled male and female|tissue:endothelial and hemogenic endothelial|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq control for double morphants endothelial hemogenic endothelial cell 26hpf replicate 1", "13", "13", "TruSeq stranded mRNA", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "PAIRED", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP226614", null, null, "RNA_seq control for double morphants endothelial_hemogenic endothelial cell 26hpf replicate 1_R1.fastq.gz RNA_seq control for double morphants endothelial_hemogenic endothelial cell 26hpf replicate 1_R2.fastq.gz", "fastq fastq", 1909021350.0, 12726809.0, "RNA seq control for double morphants endothelial hemogenic endothelial cell 26hpf replicate 1 R1.fastq.gz", "0:75 1:75", "A:536542827;C:420010389;G:423642042;T:528630203;N:195889", 75, 75, null, null, 536542827, 420010389, 423642042, 528630203, 195889, "SRX7034687", "SRS5554730", "SRA983011", "Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany|Department of Cellular and Molecular Immunology", "Max Planck Institute of Immunobiology and Epigenetics, Freiburg, Germany", 2, 0.91535, 0.91534, 0.11578, 0.11457, 0.73705, 0.74373, 0.47609, 0.47115, 75, 75, "B", "B", "biological fallback assumption", "illumina", "hiseq_era", "unknown", "size_fractionation", "trueseq", "bulk", "unknown", "unknown", null, "Germany", "2019-10-24", "Pharyngula", "Embryo", "Endothelium", "Cardiovascular System"], [55399, "SRR10323911", "SRX7034686", "SRS5554730", "SRP226614", "PRJNA578896", "Repetitive elements engage Rig I and Mda5 in interplay with Lgp2 to enhance hematopoietic stem cell emergence", "PRJNA578896", "Other", "In this study we examine the role of RIG I like receptors RLRs in hematopoietic stem and progenitor cell formation. We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. 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We have performed extensive expression analysis and chromatin accessibility assays on endothelial and hemogenic endothelial cells in knockdown animals for all the RLR receptors. Additionally we did expression analysis on animals with knockdown of two receptors. Finally we examined the upregulation of repetitive elements in hemogenic endothelial cells post treatment with valproic acid VPA or decitabine.", null, null, null, null, "danRer10 raw data", null, "strain:AB/tu|age:not applicable|sex:pooled male and female|tissue:endothelial and hemogenic endothelial|BioSampleModel:Model organism or animal", null, null, null, null, null, null, null, null, "RNA seq control for rig 1 morpholino injected endothelial hemogenic endothelial cell 26hpf replicate 1", "1", "1", "NEBNext Low Input RNA Library Prep Kit", null, null, "RNA-Seq", "TRANSCRIPTOMIC", "size fractionation", "PAIRED", "ILLUMINA", "Illumina HiSeq 3000", null, "SRP226614", null, null, "RNA_seq control for rig_1 morpholino injected endothelial_hemogenic endothelial cell 26hpf replicate 1_R1.fastq.gz RNA_seq control for rig_1 morpholino injected endothelial_hemogenic endothelial cell 26hpf replicate 1_R2.fastq.gz", "fastq fastq", 2438070600.0, 16253804.0, "RNA seq control for rig 1 morpholino 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