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Mus musculus

ABSTRACT: ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex

PROVIDER: PRJNA155343 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR285188.fastq.gz	Fastqsanger.gz
	SRR285189.fastq.gz	Fastqsanger.gz
	SRR285190.fastq.gz	Fastqsanger.gz

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Ezh2 and H3K27me3 in cardiomyocytes

Project description:This SuperSeries is composed of the following subset Series: GSE29992: Genome-wide profiling of E12.5 cardiomyocytes RNA expression in both hetozygeous control and mutant GSE29994: ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex Refer to individual Series

2012-03-15 | E-GEOD-29997 | biostudies-arrayexpress

ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex

Project description:Ezh2 and H3K27me3 binding sites in E12.5 heart apex

2012-03-15 | GSE29994 | GEO

ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex

Project description:Ezh2 and H3K27me3 binding sites in E12.5 heart apex PRC2 binding sites in wild type cardiomyocytes

2012-03-15 | E-GEOD-29994 | biostudies-arrayexpress

Mus musculus

Project description:Sap130 ChIP-seq on Mouse E12.5 heart

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Genome-wide profiling of E12.5 cardiomyocytes RNA expression in both heterozygous control and mutant

Project description:Congenital heart disease is among the most frequent major birth defects. Epigenetic marks are crucial for organogenesis, but their role in heart development is poorly understood. Polycomb Repressive Complex 2 (PRC2) trimethylates histone H3 at lysine 27, establishing H3K27me3 repressive epigenetic marks that promote tissue-specific differentiation by silencing ectopic gene programs. We studied the function of the catalytic subunit of PRC2, EZH2, in murine heart development. Early EZH2 inactivation by Nkx2-5Cre caused lethal congenital heart malformations, but slightly later EZH2 inactivation by cTNT-Cre did not. To study how the cardiomyocytes gene expression program is properly established in the early heart development, we combined the technologies of RNA sequencing and chromatin immunoprecipitation sequencing to identify the functional target genes directly repressed by EZH2. Intriguingly, these were enriched for transcriptional regulators of non-cardiac expression programs, such as transcription factors that regulate neuronal (Pax6) and cardiac progenitor genes (Isl1 and Six1). EZH2 was also required to maintain spatiotemporal regulation of cardiac gene expression, as Hcn4, Mlc2a, and Bmp10 were inappropriately upregulated in ventricular RNA. Furthermore, EZH2 was required for normal cardiomyocyte proliferation, establishing H3K27me3 epigenetic marks at cell cycle inhibitors Ink4a/b and repressing their expression. Our study reveals a previously undescribed role of EZH2 in regulating heart formation and shows that perturbation of the epigenetic landscape early cardiogenesis has sustained disruptive effects at later developmental stages. 8 E12.5 heart apex were used for RNA preparation each group.

2012-03-15 | E-GEOD-29992 | biostudies-arrayexpress

Divergent mechanisms of EZH1 regulation of heart development and regeneration [RNA-Seq]

Project description:RNA-seq for DKO, E1KO, E2KO and WT E12.5 heart revealed that EZH1 and EZH2 play a partially redundant role to trimethylate histone H3 at Lys 27 (H3K27me3). Through EZH1, H3K27me3 and H3K27ac ChIP-seq and RNA-seq for P13 EZH1 and GFP overexpressing heart (AAVEzh1 and AAVGFP respectively) suffered MI at P10, we surprisingly found that EZH1 can active the expression of regenerating relevant genes by directly binding to the promoter of targeted genes and through a mechanism independent of H3K27me3 deposition. Together, we unravel a requirement but divergent mechanisms of EZH1 in heart development and regeneration

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Repression of Igf1 expression by Ezh2 prevents basal cell differentiation in the developing lung

Project description:Gene expression (RNA-seq) and H3K27me3 binding (ChIP-seq) profiling of wild type and Ezh2-deficient mouse lung epithelium. Lungs from wild type and Ezh2-deficient mice (Ezh2 deletion is specific to lung epithelium) were collected at day e16.5. Lung cells were separated into epithelial and stromal populations based on EpCAM expression. Epithelial cells were profiled for both gene expression (Total RNA-seq) and H3K27me3 binding (ChIP-seq). Additionally, stromal cells were also profiled for gene expression.

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Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)

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Project description:This experiment sought to determine the chromatin structure and PRC2 occupancy at the promoters of all genes in mouse ESCs ChIP-seq for EZH2, SUZ12, and H3K27me3 were performed on WT E14 cells in 2 biological replicates each. In addition H3K27me3 ChIP-seq was also performed on a clone of E14 cells expressing a tagged version of EZH2, which for the purpose of this study was used as replicate #3.

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