Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

ABSTRACT: WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

PROVIDER: PRJNA438521 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6844910_1.fastq.gz	Fastqsanger.gz
	SRR6844910_2.fastq.gz	Fastqsanger.gz
	SRR6844920_1.fastq.gz	Fastqsanger.gz
	SRR6844920_2.fastq.gz	Fastqsanger.gz
	SRR6844912_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 40

Similar Datasets

WT and Hira-null undifferentiated mESCs and day15 differentiated cardiomyocytes

Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from the knockout of Hira in undifferentiated mouse embryonic stem cells (mESCs) and in day 15 differentiated cardiomyocytes.Methods: RNA extraction was done in duplicate from WT and Hira-null mESCs at day0 and day15 using TRIzol reagent. RNAseq was done onIllumina Nextseq500 and processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R2 package. Gene lists were filtered using adjusted p-value ≤ 0.05 and absolute fold change ≥ 2. Results:We identified 1680 transcripts changed in the absence of HIRA in day 15 differentiated cardiomyocytes. GO term cardiovascular system development was the most downregulated gene set(p-value ≤ 0.01 and FDR ≤0.1. Conclusion: this study analysis the role of HIRA in early cardiac mesoderm development usinf an invitro mESCs model.

2019-04-01 | GSE111910 | GEO

Genome wide enrichment of H3.3 in WT and Hira-null embryonic stem cells and day 15 differentiated cardiac progenitor

Project description:HIRA is a histone chaperone that modulates gene expression through the deposition of H3.3. Conditional knockout of Hira in embryonic mouse hearts leads to cardiac septal defects. However, the effects of HIRA on the gene expression profile at earlier stages of cardiogenic mesoderm differentiation has not yet been studied. Differentiation of mouse embryonic stem cells (mESCs) towards cardiomyocytes mimics some of these events and is an accepted model of these early stages. We performed RNA-Seq and H3.3-HA ChIP-seq on both WT and Hira-null mESCs and early cardiomyocyte progenitors of both genotypes. Analysis of our RNA-seq data showed differential down regulation of cardiovascular development-related genes in Hira-null cardiomyocytes compared to WT cardiomyocytes. Correlating these data with H3.3 enrichment showed that HIRA is required for the expression of the transcription factors (TFs) Gata6, Meis1 and Tbx2. These TFs displayed diminished HIRA-dependent H3.3 enrichment in their gene bodies or at their transcription start site in the absence of HIRA. Our results reveal new transcription factors through which HIRA influences cardiogenesis in vitro and potentially in vivo.

2019-01-18 | GSE112078 | GEO

HIRA null vs parental mES cell line

Project description:Hira has been implicated in replication-independent chromatin assembly. To determine the role of Hira in the regulation of embryonic stem (ES) cell gene expression, we used microarrays to analyze the global program of gene expression in Hira null versus WT undifferentiated ES cells.

2009-12-19 | GSE19542 | GEO

Genome-wide gene expression analysis of undifferentiated mouse embryonic stem cells (mES), neonatal mouse cardiomyocytes (CMp) and adult mouse cardiomyocytes (CMa)

Project description:Genome-wide gene expression analysis at different stages of cardiomyocyte differentiation (undifferentiated mouse embryonic stem cells, neonatal mouse cardiomyocytes and adult mouse cardiomyocytes). Results provide important information on the differential expressed genes between undifferentiated mouse embrionic stem cells (mES) and mouse cardiomyocytes (CM) and also between cardiomyocytes from neonatal (CMp) and adult stages (CMa). This dataset allowed us to compare the expression profile of mES, CMp and CMa with the epigenetic profile of histone methylation generated with ChIP-seq experiments. Total RNA was obtained from biological triplicate of undifferentiated mouse embryonic stem cells (mES), neonatal mouse cardiomyocytes (CMp) and adult mouse cardiomyocytes (CMa)

2014-12-22 | E-GEOD-44829 | biostudies-arrayexpress

Genome-wide gene expression analysis of undifferentiated mouse embryonic stem cells (mES), neonatal mouse cardiomyocytes (CMp) and adult mouse cardiomyocytes (CMa)

2014-12-22 | GSE44829 | GEO

Effect of a cardiomyocyte-specific Hira conditional knockout on gene expression in the heart

Project description:We performed gene expression profiling by microarray using RNA extracted from healthy free wall left ventricle tissues from control and Hira cardiomyocyte-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed regions. Conditional knockout of Hira in cardiomyocytes resulted in impaired cardiac function, cardiomyocyte degeneration and focal replacement fibrosis. These results illustrate the role of Hira in controlling the cardiac gene program. 4 animals per group (control and Hira conditional knockout) hybridized in triplicate. RNA was extracted from healthy free wall left ventricle.

2016-04-06 | E-GEOD-71833 | biostudies-arrayexpress

Effect of a cardiomyocyte-specific Hira conditional knockout on gene expression in the heart

2016-04-06 | GSE71833 | GEO

Analysis of isotope incorporation in differentiated and undifferentiated podocytes

Project description:We subjected podocytes (either differentiated or undifferentiated) to a pulse with stable isotope labeled amino acids for 24, 48, 72 and 96h.

2018-05-01 | PXD006887 | Pride

Stem Cells Secrete Factors That Induce Proliferation In Differentiated Cardiomyocytes

Project description:Media conditioned by undifferentiated human embryonic stem cells enhanced karyokinesis, cytokinesis and cell proliferation in cultures of differentiated, beating primary rat cardiomyocytes without altering their final contractile phenotype. Transcriptome analysis of proliferating cardiomyocytes revealed comprehensive activation of the ROCK 1 and 2 G-protein coupled receptor (GPCR) pathway associated with cytokinesis, and the RAS/RAF/MEK/ERK receptor tyrosine kinase pathways (RTK) and JAK/STAT-cytokine pathway involved in cell cycle progression. Correlative multi-analyte profiling (85 proteins) of conditioned media identified 33 proteins at significantly elevated levels compared to unconditioned media including ligands specific to the GPCR signal transduction pathways (serum amyloid A, monocyte chemoattractant protein-1, macrophage inhibitory protein, IL-8, macrophage inflammatory protein 1-alpha, eotaxin), RTK activation (IGFbp-1, IGFbp-2, HGF) and JAK-STAT stimulation pathways (IL-6, IFNa) activated in the treated cardiomyocytes. These data indicated that ES cells secreted a unique admixture of factors associated with induction of mitotic replication, cytokinesis and proliferation in cardiomyocytes.

2010-06-01 | GSE13708 | GEO

PHB Acts as a Member of the HIRA Complex to Control an Epigenetic and Metabolic Circuitry

Project description:Cellular metabolism and chromatin landscape both contribute to cell fate determination. However, their interplay remains poorly understood. Here we show that Prohibitin (PHB), an evolutionarily conserved protein, involves in a histone variant H3.3 chaperon HIRA complex-dependent epigenetic and metabolic circuitry to maintain the identity of human embryonic stem cells (hESCs). We found that silencing of PHB triggers hESC differentiation with concomitant enhancements of histone 3 (H3) lysine (K) methyl modifications as a result of the reduced production of Î±-ketoglutarate (Î±-KG), a metabolite required for activities of many dioxygenase and in turn chromatin structure1,2. Mechanistically, PHB acts as a functional member of the HIRA complex3,4. Resembling PHB deficiency, loss of HIRA in hESCs leads to massive differentiation and aberrant histone modifications, although it was previously found not to disrupt the self-renewal in mouse ESCs (mESCs)5. Genome-wide H3.3 ChIP- sequence analyses indicate that reduction of H3.3 deposition caused by PHB knock down is extremely similar to that induced by HIRA knock down. Specifically, silencing either HIRA or PHB leads to repressive chromatin characters at promoters of pluripotency genes and isocitrate dehydrogenases (IDHs), the enzyme responsible for Î±-KG production, but active chromatin features at promoters of developmental genes, paralleling to transcript levels of these genes. Our results identify PHB as an essential factor not only for hESC self-renewal but also for the proper function of the HIRA complex, linking the HIRA complex-dependent H3.3 deposition to the production of a critical metabolite required for shaping chromatin structure, and demonstrating the importance of the interplay between epigenetic state and metabolic regulation in cell fate determination. Examination of H3.3 deposition in NT, PHB, and HIRA siRNA treated hESCs respectively.

2016-08-11 | E-GEOD-72143 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data