metadata: run_metadata: 21 rows where experiment.library_source = "TRANSCRIPTOMIC", experiment.library_strategy = "OTHER" and tissue_curation

21 rows where experiment.library_source = "TRANSCRIPTOMIC", experiment.library_strategy = "OTHER" and tissue_curation_coarse = "Cardiovascular System"

descending

Link	rowid ▼	run.accession	experiment.accession	sample.accession	study.accession	bioproject	study.title	study.alias	study.type	study.abstract	study.PMIDs	sample.title	sample.alias	sample.attributes	GEOsample.title	GEOsample.dataprocessing	GEOsample.source	GEOsample.extractprotocol	GEOsample.growthprotocol	GEOsample.characteristics	GEOsample.accession	experiment.title	experiment.alias	experiment.library_name	experiment.design_description	experiment.library_construction_protocol	experiment.library_strategy	experiment.library_source	experiment.library_selection	experiment.library_layout	experiment.platform	experiment.instrument_model	experiment.study_ref	run.filename	run.semantic_name	run.total_bases	run.total_spots	run.alias	run.read_lengths	run.base_counts	run.r1_length	run.r2_length	run.Acount	run.Ccount	run.Gcount	run.Tcount	run.Ncount	run.experiment	run.pool_member	submission.accession	submission.srasource	submission.bioprojectsource	seqdetective.n_mates	seqdetective.mapping_rate.mate1	seqdetective.nofeature_rate.mate1	seqdetective.sparsity.mate1	seqdetective.pos_strand_rate.mate1	seqdetective.readlen.mate1	seqdetective.judgement.mate1	seqdetective.judgement.reason	platform_family	instrument_generation	read_bias	selection_class	prep_kit	sc_or_bulk	tech_class	technology	submission.bioprojectsource.country	earliest_date	devstage_curation	devstage_curation_coarse	tissue_curation	tissue_curation_coarse
41827	41827	SRR5251446	SRX2557171	SRS1974564	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR139 B1	nicoli mutmir AG01645	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 139\|replicate:1\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR139 B1	AG01645.1	AG01645.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01645.1_R1.fastq.gz	fastq	1574284140.0	20714265.0	AG01645.1 R1.fastq.gz	0:76	A:485471345;C:270854124;G:374164721;T:443766613;N:27337	76		485471345	270854124	374164721	443766613	27337	SRX2557171	SRS1974564	SRA537606	Yale University\|Genetics	Yale University	1	0.82142	0.14068	0.8002	0.5444	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-27	Undetermined	Embryo	Endothelium	Cardiovascular System
41828	41828	SRR5251445	SRX2557170	SRS1974563	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR139 B2	nicoli mutmir AG01646	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 139\|replicate:2\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR139 B2	AG01646.1	AG01646.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01646.1_R1.fastq.gz	fastq	1484740104.0	19536054.0	AG01646.1 R1.fastq.gz	0:76	A:453388316;C:246477203;G:365031959;T:419816346;N:26280	76		453388316	246477203	365031959	419816346	26280	SRX2557170	SRS1974563	SRA537606	Yale University\|Genetics	Yale University	1	0.82649	0.1897	0.79862	0.52759	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41829	41829	SRR5251444	SRX2557169	SRS1974562	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR139 B3	nicoli mutmir AG01647	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 139\|replicate:3\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR139 B3	AG01647.1	AG01647.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01647.1_R1.fastq.gz	fastq	881298660.0	11596035.0	AG01647.1 R1.fastq.gz	0:76	A:270675838;C:160127586;G:228157662;T:222301246;N:36328	76		270675838	160127586	228157662	222301246	36328	SRX2557169	SRS1974562	SRA537606	Yale University\|Genetics	Yale University	1	0.76133	0.15034	0.83341	0.56596	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41830	41830	SRR5251443	SRX2557168	SRS1974561	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR139 B1	nicoli mutmir AG01648	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 139 ya302/ya302\|molecule:mRNA\|condition:miR 139\|replicate:1\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR139 B1	AG01648.1	AG01648.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01648.1_R1.fastq.gz	fastq	637896880.0	8393380.0	AG01648.1 R1.fastq.gz	0:76	A:192829278;C:112701153;G:153321271;T:179019095;N:26083	76		192829278	112701153	153321271	179019095	26083	SRX2557168	SRS1974561	SRA537606	Yale University\|Genetics	Yale University	1	0.75971	0.1181	0.82171	0.56797	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41831	41831	SRR5251442	SRX2557167	SRS1974560	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR139 B2	nicoli mutmir AG01649	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 139 ya302/ya302\|molecule:mRNA\|condition:miR 139\|replicate:2\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR139 B2	AG01649.1	AG01649.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01649.1_R1.fastq.gz	fastq	849868328.0	11182478.0	AG01649.1 R1.fastq.gz	0:76	A:258225905;C:148467172;G:205165181;T:237974100;N:35970	76		258225905	148467172	205165181	237974100	35970	SRX2557167	SRS1974560	SRA537606	Yale University\|Genetics	Yale University	1	0.75096	0.14506	0.81507	0.5545	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41832	41832	SRR5251441	SRX2557166	SRS1974559	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR139 B3	nicoli mutmir AG01650	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 139 ya302/ya302\|molecule:mRNA\|condition:miR 139\|replicate:3\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR139 B3	AG01650.1	AG01650.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01650.1_R1.fastq.gz	fastq	998464668.0	13137693.0	AG01650.1 R1.fastq.gz	0:76	A:311526420;C:176545041;G:251852786;T:258497630;N:42791	76		311526420	176545041	251852786	258497630	42791	SRX2557166	SRS1974559	SRA537606	Yale University\|Genetics	Yale University	1	0.76479	0.11192	0.82674	0.54621	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41833	41833	SRR5251440	SRX2557165	SRS1974558	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR24 B1	nicoli mutmir AG01651	strain:TU/AB\|age:51.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 24\|replicate:1\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR24 B1	AG01651.1	AG01651.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01651.1_R1.fastq.gz	fastq	570492252.0	7506477.0	AG01651.1 R1.fastq.gz	0:76	A:162512811;C:104071716;G:135730697;T:168149427;N:27601	76		162512811	104071716	135730697	168149427	27601	SRX2557165	SRS1974558	SRA537606	Yale University\|Genetics	Yale University	1	0.73988	0.10157	0.86647	0.54252	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41834	41834	SRR5251439	SRX2557164	SRS1974557	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR24 B2	nicoli mutmir AG01652	strain:TU/AB\|age:51.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 24\|replicate:2\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR24 B2	AG01652.1	AG01652.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01652.1_R1.fastq.gz	fastq	1072886148.0	14116923.0	AG01652.1 R1.fastq.gz	0:76	A:338399596;C:192703439;G:242960887;T:298769761;N:52465	76		338399596	192703439	242960887	298769761	52465	SRX2557164	SRS1974557	SRA537606	Yale University\|Genetics	Yale University	1	0.76456	0.11024	0.89197	0.59214	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41835	41835	SRR5251438	SRX2557163	SRS1974556	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR24 B3	nicoli mutmir AG01653	strain:TU/AB\|age:51.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 24\|replicate:3\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR24 B3	AG01653.1	AG01653.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01653.1_R1.fastq.gz	fastq	1016374144.0	13373344.0	AG01653.1 R1.fastq.gz	0:76	A:310958343;C:168702106;G:223420046;T:313241363;N:52286	76		310958343	168702106	223420046	313241363	52286	SRX2557163	SRS1974556	SRA537606	Yale University\|Genetics	Yale University	1	0.75735	0.12224	0.79756	0.55136	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-02-13	Undetermined	Embryo	Endothelium	Cardiovascular System
41836	41836	SRR5251437	SRX2557162	SRS1974555	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR24 B1	nicoli mutmir AG01654	strain:TU/AB\|age:51.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 24 ya324/? ya325/? ya326/? ya327/?\|molecule:mRNA\|condition:miR 24\|replicate:1\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR24 B1	AG01654.1	AG01654.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01654.1_R1.fastq.gz	fastq	782170112.0	10291712.0	AG01654.1 R1.fastq.gz	0:76	A:238316720;C:132163709;G:179301544;T:232350598;N:37541	76		238316720	132163709	179301544	232350598	37541	SRX2557162	SRS1974555	SRA537606	Yale University\|Genetics	Yale University	1	0.7683	0.10712	0.80034	0.55804	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41837	41837	SRR5251436	SRX2557161	SRS1974554	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR24 B2	nicoli mutmir AG01655	strain:TU/AB\|age:51.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 24 ya324/? ya325/? ya326/? ya327/?\|molecule:mRNA\|condition:miR 24\|replicate:2\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR24 B2	AG01655.1	AG01655.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01655.1_R1.fastq.gz	fastq	1053946340.0	13867715.0	AG01655.1 R1.fastq.gz	0:76	A:318351311;C:191163031;G:240348413;T:304030367;N:53218	76		318351311	191163031	240348413	304030367	53218	SRX2557161	SRS1974554	SRA537606	Yale University\|Genetics	Yale University	1	0.77588	0.07983	0.83934	0.56228	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41838	41838	SRR5251435	SRX2557160	SRS1974553	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR24 B3	nicoli mutmir AG01656	strain:TU/AB\|age:51.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 24 ya324/? ya325/? ya326/? ya327/?\|molecule:mRNA\|condition:miR 24\|replicate:3\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR24 B3	AG01656.1	AG01656.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01656.1_R1.fastq.gz	fastq	1182467736.0	15558786.0	AG01656.1 R1.fastq.gz	0:76	A:344465226;C:204677242;G:269228338;T:364036735;N:60195	76		344465226	204677242	269228338	364036735	60195	SRX2557160	SRS1974553	SRA537606	Yale University\|Genetics	Yale University	1	0.78956	0.13495	0.81517	0.56342	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-02-13	Undetermined	Embryo	Endothelium	Cardiovascular System
41839	41839	SRR5251434	SRX2557159	SRS1974552	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR223 B1	nicoli mutmir AG01657	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 223\|replicate:1\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR223 B1	AG01657.1	AG01657.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01657.1_R1.fastq.gz	fastq	536336712.0	7057062.0	AG01657.1 R1.fastq.gz	0:76	A:158301607;C:93070120;G:121382262;T:163555487;N:27236	76		158301607	93070120	121382262	163555487	27236	SRX2557159	SRS1974552	SRA537606	Yale University\|Genetics	Yale University	1	0.76425	0.1278	0.84222	0.55305	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-02-13	Undetermined	Embryo	Endothelium	Cardiovascular System
41840	41840	SRR5251433	SRX2557158	SRS1974551	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR223 B2	nicoli mutmir AG01658	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 223\|replicate:2\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR223 B2	AG01658.1	AG01658.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01658.1_R1.fastq.gz	fastq	798581856.0	10507656.0	AG01658.1 R1.fastq.gz	0:76	A:241352089;C:134327379;G:183394123;T:239469845;N:38420	76		241352089	134327379	183394123	239469845	38420	SRX2557158	SRS1974551	SRA537606	Yale University\|Genetics	Yale University	1	0.76221	0.13398	0.82459	0.55228	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41841	41841	SRR5251432	SRX2557157	SRS1974550	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs WT miR223 B3	nicoli mutmir AG01659	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|molecule:mRNA\|condition:miR 223\|replicate:3\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs WT miR223 B3	AG01659.1	AG01659.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01659.1_R1.fastq.gz	fastq	1093998948.0	14394723.0	AG01659.1 R1.fastq.gz	0:76	A:330741822;C:186325335;G:249557623;T:327320449;N:53719	76		330741822	186325335	249557623	327320449	53719	SRX2557157	SRS1974550	SRA537606	Yale University\|Genetics	Yale University	1	0.77108	0.14674	0.80955	0.55819	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
41842	41842	SRR5251431	SRX2557156	SRS1974549	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR223 B1	nicoli mutmir AG01660	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 223 ya304/ya304\|molecule:mRNA\|condition:miR 223\|replicate:1\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR223 B1	AG01660.1	AG01660.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01660.1_R1.fastq.gz	fastq	849905492.0	11182967.0	AG01660.1 R1.fastq.gz	0:76	A:250953875;C:146191904;G:190040699;T:262674911;N:44103	76		250953875	146191904	190040699	262674911	44103	SRX2557156	SRS1974549	SRA537606	Yale University\|Genetics	Yale University	1	0.7687	0.14192	0.82842	0.5344	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-02-13	Undetermined	Embryo	Endothelium	Cardiovascular System
41843	41843	SRR5251430	SRX2557155	SRS1974548	SRP099466	PRJNA374579	microRNAs Establish Uniform Traits during the Architecture of Vertebrate Embryos	PRJNA374579	Other	Proper functioning of an organism requires cells and tissues to behave in uniform well organized ways. How this optimum of phenotypes is achieved during the development of vertebrates is unclear. Here we carried out a multifaceted and single cell resolution screen of zebrafish embryonic blood vessels upon mutagenesis of single and multi gene miRNA families. We found that embryos lacking particular miRNA dependent signaling pathways develop a vascular trait similar to wild type but with a profound increase in phenotypic heterogeneity. Aberrant trait variance in miRNA mutant embryos uniquely sensitizes their vascular system to environmental perturbations. We uncovered a previously unrecognized role for specific vertebrate miRNAs to protect tissue development against phenotypic variability. This discovery marks an important advance in our comprehension of how miRNAs function in the development of higher organisms.		QuantSeq mutant miRNAs Mut miR223 B2	nicoli mutmir AG01661	strain:TU/AB\|age:27.0\|sex:pooled male and female\|tissue:endothelial cells\|genotype:miR 223 ya304/ya304\|molecule:mRNA\|condition:miR 223\|replicate:2\|BioSampleModel:Model organism or animal								QuantSeq mutant miRNAs Mut miR223 B2	AG01661.1	AG01661.1	1		OTHER	TRANSCRIPTOMIC	unspecified	SINGLE	ILLUMINA	Illumina HiSeq 2000	SRP099466	AG01661.1_R1.fastq.gz	fastq	840115400.0	11054150.0	AG01661.1 R1.fastq.gz	0:76	A:257057495;C:141775085;G:188281166;T:252960590;N:41064	76		257057495	141775085	188281166	252960590	41064	SRX2557155	SRS1974548	SRA537606	Yale University\|Genetics	Yale University	1	0.74292	0.10759	0.83615	0.55136	76	B	usable mapping rate	illumina	hiseq_era	unknown	small_rna	lexogen	bulk	unknown	unknown	United States	2017-03-28	Undetermined	Embryo	Endothelium	Cardiovascular System
71064	71064	SRR21218373	SRX17229104	SRS14795570	SRP394145	PRJNA872137	The Translation Initiation Factor Homolog eif4e1c Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.	GSE211793	Other	The?eIF4E family of translation initiation factors bind five prime methylated caps and act as the limiting step for mRNA translation. The canonical eIF4E1A is required for cell viability yet other related families exist and are all utilized in specific contexts or tissues. Here we describe a new family called Eif4e1c that is ancestral to the canonical eIF4E1A in vertebrates and for which we find roles during heart development and regeneration in zebrafish.?The Eif4e1c family is present in all aquatic vertebrates but has been lost in all terrestrial species. A core group of amino acids shared over 500 million yrs of evolution from?ray finned fish to sharks?forms an evolutionarily conserved binding interface along the surface of the protein suggesting Eif4e1c functions in a novel pathway.? Deletion of eif4e1c?in zebrafish caused growth deficits and impaired survival in juveniles.?Mutants surviving to maturity had fewer cardiomyocytes while also showing reduced proliferative responses to cardiac injury. Ribosome profiling of mutant hearts demonstrated changes in translation efficiency of mRNA for genes known to regulate cardiomyocyte proliferation. Although?eif4e1c?is expressed in many tissues and is the predominant cap binding initiation homolog in embryos its disruption had most notable impact on the heart and at juvenile stages. ?Our findings reveal context dependent requirements for translation initiation regulators during heart regeneration. Overall design: Ribosome profiling of adult uninjured eif4e1c zebrafish mutant hearts and adult uninjured EK zebrafish wildtype hearts.	pubmed:37306388	zebrafish Ribo seq Eif4e1c / rep2 [r mR2]	GSM6502516	source name:heart\|tissue:heart\|cell line:Mutant\|genotype:Eif4e1c /	zebrafish Ribo seq Eif4e1c / rep2 [r mR2]	Fastq files were processed using FastQC v0.11.8; RRID:SCR 014583 for quality control QC analysis. Pre processing of sequencing reads was based on the QC report using the FASTQ Quality Filter module in the FASTX Toolkit RRID:SCR 019035. This was used to filter the bases with 99% accuracy based on Q Score. Reads were removed that showed less than 70% of nucleotides with an accuracy of at least 99%. The sequences were collapsed according to their by Unique Molecular Identifiers UMIs. Cutadapt RRID:SCR 011841 was used to trim 21 nt adaptor before the first nt and the last 4 nt from the reads to remove the UMI. The processed reads were aligned to GRCz11/danRer11 assembly of the zebrafish genome; Genome Reference Consortium using STAR v2.5.3a RRID:SCR 004463. Generated bam files were processed with RiboProfiling package v1.2.2. Coverage counts on the coding regions CDS were obtained for each sample based on RiboProfiling function modules TxDb.Drerio.UCSC.danRer11.refGene v3.4.6; Annotation package for TxDb objects; Team BC 2019 and GenomicFeatures package v1.46.1. Differential expression analysis was performed using the DESeq2 pipeline version 1.26.0 based on the expressed raw reads. Assembly: GRCz11/danRer11 Library strategy: Ribo seq	heart	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer’s instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	Zebrafish used for ribosome profiling were grown together under normal conditions and were genotyped upon reaching maturity.	tissue:heart\|cell line:Mutant\|genotype:Eif4e1c /	GSM6502516	GSM6502516: zebrafish Ribo seq Eif4e1c / rep2 [r mR2]; Danio rerio; OTHER	GSM6502516 r1	GSM6502516	1	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer's instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	OTHER	TRANSCRIPTOMIC	other	SINGLE	ILLUMINA	NextSeq 550	SRP394145	rS4_mR2.fastq.gz	fastq	6611131472.0	86988572.0	GSM6502516 r1	0:76 1:0	A:1748359123;C:1658689534;G:1706027528;T:1497702781;N:352506	76	0	1748359123	1658689534	1706027528	1497702781	352506	SRX17229104	SRS14795570	SRA1485233	Biological Chemistry and Pharmacology, The Ohio State University	Biological Chemistry and Pharmacology, The Ohio State University	1	0.0	0.0	1.0		76	T	under 1.2% mapping rate	illumina	nextseq	unknown	other	unknown	bulk	unknown	unknown	United States	2022-08-22	Undetermined	Multi-stage	Heart	Cardiovascular System
71065	71065	SRR21218374	SRX17229103	SRS14795569	SRP394145	PRJNA872137	The Translation Initiation Factor Homolog eif4e1c Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.	GSE211793	Other	The?eIF4E family of translation initiation factors bind five prime methylated caps and act as the limiting step for mRNA translation. The canonical eIF4E1A is required for cell viability yet other related families exist and are all utilized in specific contexts or tissues. Here we describe a new family called Eif4e1c that is ancestral to the canonical eIF4E1A in vertebrates and for which we find roles during heart development and regeneration in zebrafish.?The Eif4e1c family is present in all aquatic vertebrates but has been lost in all terrestrial species. A core group of amino acids shared over 500 million yrs of evolution from?ray finned fish to sharks?forms an evolutionarily conserved binding interface along the surface of the protein suggesting Eif4e1c functions in a novel pathway.? Deletion of eif4e1c?in zebrafish caused growth deficits and impaired survival in juveniles.?Mutants surviving to maturity had fewer cardiomyocytes while also showing reduced proliferative responses to cardiac injury. Ribosome profiling of mutant hearts demonstrated changes in translation efficiency of mRNA for genes known to regulate cardiomyocyte proliferation. Although?eif4e1c?is expressed in many tissues and is the predominant cap binding initiation homolog in embryos its disruption had most notable impact on the heart and at juvenile stages. ?Our findings reveal context dependent requirements for translation initiation regulators during heart regeneration. Overall design: Ribosome profiling of adult uninjured eif4e1c zebrafish mutant hearts and adult uninjured EK zebrafish wildtype hearts.	pubmed:37306388	zebrafish Ribo seq Eif4e1c / rep 1 [r mR1]	GSM6502515	source name:heart\|tissue:heart\|cell line:Mutant\|genotype:Eif4e1c /	zebrafish Ribo seq Eif4e1c / rep 1 [r mR1]	Fastq files were processed using FastQC v0.11.8; RRID:SCR 014583 for quality control QC analysis. Pre processing of sequencing reads was based on the QC report using the FASTQ Quality Filter module in the FASTX Toolkit RRID:SCR 019035. This was used to filter the bases with 99% accuracy based on Q Score. Reads were removed that showed less than 70% of nucleotides with an accuracy of at least 99%. The sequences were collapsed according to their by Unique Molecular Identifiers UMIs. Cutadapt RRID:SCR 011841 was used to trim 21 nt adaptor before the first nt and the last 4 nt from the reads to remove the UMI. The processed reads were aligned to GRCz11/danRer11 assembly of the zebrafish genome; Genome Reference Consortium using STAR v2.5.3a RRID:SCR 004463. Generated bam files were processed with RiboProfiling package v1.2.2. Coverage counts on the coding regions CDS were obtained for each sample based on RiboProfiling function modules TxDb.Drerio.UCSC.danRer11.refGene v3.4.6; Annotation package for TxDb objects; Team BC 2019 and GenomicFeatures package v1.46.1. Differential expression analysis was performed using the DESeq2 pipeline version 1.26.0 based on the expressed raw reads. Assembly: GRCz11/danRer11 Library strategy: Ribo seq	heart	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer’s instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	Zebrafish used for ribosome profiling were grown together under normal conditions and were genotyped upon reaching maturity.	tissue:heart\|cell line:Mutant\|genotype:Eif4e1c /	GSM6502515	GSM6502515: zebrafish Ribo seq Eif4e1c / rep 1 [r mR1]; Danio rerio; OTHER	GSM6502515 r1	GSM6502515	1	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer's instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	OTHER	TRANSCRIPTOMIC	other	SINGLE	ILLUMINA	NextSeq 550	SRP394145	rS3_mR1.fastq.gz	fastq	13677356644.0	179965219.0	GSM6502515 r1	0:76 1:0	A:3346749848;C:3412648254;G:3629003006;T:3288222747;N:732789	76	0	3346749848	3412648254	3629003006	3288222747	732789	SRX17229103	SRS14795569	SRA1485233	Biological Chemistry and Pharmacology, The Ohio State University	Biological Chemistry and Pharmacology, The Ohio State University	1	0.0	0.0	1.0		76	T	under 1.2% mapping rate	illumina	nextseq	unknown	other	unknown	bulk	unknown	unknown	United States	2022-08-22	Undetermined	Multi-stage	Heart	Cardiovascular System
71066	71066	SRR21218377	SRX17229102	SRS14795568	SRP394145	PRJNA872137	The Translation Initiation Factor Homolog eif4e1c Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.	GSE211793	Other	The?eIF4E family of translation initiation factors bind five prime methylated caps and act as the limiting step for mRNA translation. The canonical eIF4E1A is required for cell viability yet other related families exist and are all utilized in specific contexts or tissues. Here we describe a new family called Eif4e1c that is ancestral to the canonical eIF4E1A in vertebrates and for which we find roles during heart development and regeneration in zebrafish.?The Eif4e1c family is present in all aquatic vertebrates but has been lost in all terrestrial species. A core group of amino acids shared over 500 million yrs of evolution from?ray finned fish to sharks?forms an evolutionarily conserved binding interface along the surface of the protein suggesting Eif4e1c functions in a novel pathway.? Deletion of eif4e1c?in zebrafish caused growth deficits and impaired survival in juveniles.?Mutants surviving to maturity had fewer cardiomyocytes while also showing reduced proliferative responses to cardiac injury. Ribosome profiling of mutant hearts demonstrated changes in translation efficiency of mRNA for genes known to regulate cardiomyocyte proliferation. Although?eif4e1c?is expressed in many tissues and is the predominant cap binding initiation homolog in embryos its disruption had most notable impact on the heart and at juvenile stages. ?Our findings reveal context dependent requirements for translation initiation regulators during heart regeneration. Overall design: Ribosome profiling of adult uninjured eif4e1c zebrafish mutant hearts and adult uninjured EK zebrafish wildtype hearts.	pubmed:37306388	zebrafish Ribo seq Eif4e1c +/+ rep 2 [r pR2]	GSM6502514	source name:heart\|tissue:heart\|cell line:Wt\|genotype:Eif4e1c +/+	zebrafish Ribo seq Eif4e1c +/+ rep 2 [r pR2]	Fastq files were processed using FastQC v0.11.8; RRID:SCR 014583 for quality control QC analysis. Pre processing of sequencing reads was based on the QC report using the FASTQ Quality Filter module in the FASTX Toolkit RRID:SCR 019035. This was used to filter the bases with 99% accuracy based on Q Score. Reads were removed that showed less than 70% of nucleotides with an accuracy of at least 99%. The sequences were collapsed according to their by Unique Molecular Identifiers UMIs. Cutadapt RRID:SCR 011841 was used to trim 21 nt adaptor before the first nt and the last 4 nt from the reads to remove the UMI. The processed reads were aligned to GRCz11/danRer11 assembly of the zebrafish genome; Genome Reference Consortium using STAR v2.5.3a RRID:SCR 004463. Generated bam files were processed with RiboProfiling package v1.2.2. Coverage counts on the coding regions CDS were obtained for each sample based on RiboProfiling function modules TxDb.Drerio.UCSC.danRer11.refGene v3.4.6; Annotation package for TxDb objects; Team BC 2019 and GenomicFeatures package v1.46.1. Differential expression analysis was performed using the DESeq2 pipeline version 1.26.0 based on the expressed raw reads. Assembly: GRCz11/danRer11 Library strategy: Ribo seq	heart	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer’s instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	Zebrafish used for ribosome profiling were grown together under normal conditions and were genotyped upon reaching maturity.	tissue:heart\|cell line:Wt\|genotype:Eif4e1c +/+	GSM6502514	GSM6502514: zebrafish Ribo seq Eif4e1c +/+ rep 2 [r pR2]; Danio rerio; OTHER	GSM6502514 r1	GSM6502514	1	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer's instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	OTHER	TRANSCRIPTOMIC	other	SINGLE	ILLUMINA	NextSeq 550	SRP394145	rS2_pR2.fastq.gz	fastq	8919983048.0	117368198.0	GSM6502514 r1	0:76 1:0	A:2208663451;C:2257902067;G:2371468879;T:2081476473;N:472178	76	0	2208663451	2257902067	2371468879	2081476473	472178	SRX17229102	SRS14795568	SRA1485233	Biological Chemistry and Pharmacology, The Ohio State University	Biological Chemistry and Pharmacology, The Ohio State University	1	1e-05	0.0	0.99997	1.0	76	T	under 1.2% mapping rate	illumina	nextseq	unknown	other	unknown	bulk	unknown	unknown	United States	2022-08-22	Undetermined	Multi-stage	Heart	Cardiovascular System
71067	71067	SRR21218378	SRX17229101	SRS14795567	SRP394145	PRJNA872137	The Translation Initiation Factor Homolog eif4e1c Regulates Cardiomyocyte Metabolism and Proliferation During Heart Regeneration.	GSE211793	Other	The?eIF4E family of translation initiation factors bind five prime methylated caps and act as the limiting step for mRNA translation. The canonical eIF4E1A is required for cell viability yet other related families exist and are all utilized in specific contexts or tissues. Here we describe a new family called Eif4e1c that is ancestral to the canonical eIF4E1A in vertebrates and for which we find roles during heart development and regeneration in zebrafish.?The Eif4e1c family is present in all aquatic vertebrates but has been lost in all terrestrial species. A core group of amino acids shared over 500 million yrs of evolution from?ray finned fish to sharks?forms an evolutionarily conserved binding interface along the surface of the protein suggesting Eif4e1c functions in a novel pathway.? Deletion of eif4e1c?in zebrafish caused growth deficits and impaired survival in juveniles.?Mutants surviving to maturity had fewer cardiomyocytes while also showing reduced proliferative responses to cardiac injury. Ribosome profiling of mutant hearts demonstrated changes in translation efficiency of mRNA for genes known to regulate cardiomyocyte proliferation. Although?eif4e1c?is expressed in many tissues and is the predominant cap binding initiation homolog in embryos its disruption had most notable impact on the heart and at juvenile stages. ?Our findings reveal context dependent requirements for translation initiation regulators during heart regeneration. Overall design: Ribosome profiling of adult uninjured eif4e1c zebrafish mutant hearts and adult uninjured EK zebrafish wildtype hearts.	pubmed:37306388	zebrafish Ribo seq Eif4e1c +/+ rep 1 [r pR1]	GSM6502513	source name:heart\|tissue:heart\|cell line:Wt\|genotype:Eif4e1c +/+	zebrafish Ribo seq Eif4e1c +/+ rep 1 [r pR1]	Fastq files were processed using FastQC v0.11.8; RRID:SCR 014583 for quality control QC analysis. Pre processing of sequencing reads was based on the QC report using the FASTQ Quality Filter module in the FASTX Toolkit RRID:SCR 019035. This was used to filter the bases with 99% accuracy based on Q Score. Reads were removed that showed less than 70% of nucleotides with an accuracy of at least 99%. The sequences were collapsed according to their by Unique Molecular Identifiers UMIs. Cutadapt RRID:SCR 011841 was used to trim 21 nt adaptor before the first nt and the last 4 nt from the reads to remove the UMI. The processed reads were aligned to GRCz11/danRer11 assembly of the zebrafish genome; Genome Reference Consortium using STAR v2.5.3a RRID:SCR 004463. Generated bam files were processed with RiboProfiling package v1.2.2. Coverage counts on the coding regions CDS were obtained for each sample based on RiboProfiling function modules TxDb.Drerio.UCSC.danRer11.refGene v3.4.6; Annotation package for TxDb objects; Team BC 2019 and GenomicFeatures package v1.46.1. Differential expression analysis was performed using the DESeq2 pipeline version 1.26.0 based on the expressed raw reads. Assembly: GRCz11/danRer11 Library strategy: Ribo seq	heart	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer’s instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	Zebrafish used for ribosome profiling were grown together under normal conditions and were genotyped upon reaching maturity.	tissue:heart\|cell line:Wt\|genotype:Eif4e1c +/+	GSM6502513	GSM6502513: zebrafish Ribo seq Eif4e1c +/+ rep 1 [r pR1]; Danio rerio; OTHER	GSM6502513 r1	GSM6502513	1	The hearts were lysed on ice with 100ul of lysis buffer with 53 mg/ml cycloheximide using mechanical homogenization with a pestle for thirty seconds. Cells were lysed further by trituration of the sample using a 27.5 gauge needle syringe 20x on ice. Cell extracts average OD 7 were treated with MNase NEB CaCl2 5mM final concentration and Turbo DNAse I Invitrogen at 25°C for 30 minutes. MNase digestion was stopped with SUPERase inhibitor incubation on ice. 80S ribosomes were isolated using SH400 spin columns Cytiva. Columns were prepared according to the manufacturer's instructions. 100 µls of MNase treated sample was loaded per column and centrifuged for 2 min at 600 RCF. The flow through was isolated and incubated for 5 min. with 3x volume of Trizol LS Ambion. 200 µl of chloroform was added and incubated for 2 min. Samples were centrifuged for 15 min. at 12 000 rpm 4°C. The aqueous phase was extracted and precipitated overnight at 20°C using glycoblue ThermoFisher and isopropanol followed by centrifugation for 30 minutes at 4C at 10 000 RPM. Pellets were washed with 75% Ethanol and resuspended into RNase free water. Next Flex smRNA seq kit v3	OTHER	TRANSCRIPTOMIC	other	SINGLE	ILLUMINA	NextSeq 550	SRP394145	rS1_pR1.fastq.gz	fastq	8551941876.0	112525551.0	GSM6502513 r1	0:76 1:0	A:2015417703;C:2191682962;G:2364697448;T:1979683824;N:459939	76	0	2015417703	2191682962	2364697448	1979683824	459939	SRX17229101	SRS14795567	SRA1485233	Biological Chemistry and Pharmacology, The Ohio State University	Biological Chemistry and Pharmacology, The Ohio State University	1	1e-05	0.0	0.99997	0.0	76	T	under 1.2% mapping rate	illumina	nextseq	unknown	other	unknown	bulk	unknown	unknown	United States	2022-08-22	Undetermined	Multi-stage	Heart	Cardiovascular System

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