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Polycomb-dependent H3K27me1 and H3K27me2 characterization in mouse ES cells (E14 and E36 with H3K27me1/2 and H3)

ABSTRACT: These data include the genome wide location analysis of H3K27me1/2/ac and H3K4me1/3 by ChIP in mouse ES cells. Precipitation of formaldehyde cross-linked chromatin prepared from mouse ES cell using specific antibodies against Histone H3 and its specific modifications. Rabbit IgG were used as control.

ORGANISM(S): Mus musculus

SUBMITTER: Sri Ganesh Jammula

PROVIDER: E-GEOD-40109 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Polycomb-dependent H3K27me1 and H3K27me2 characterization in mouse ES cells (E36 with H3K27ac, H3K27me1, and H3K4me1/3)

Project description:These data include the genome wide location analysis of H3K27me1/2/ac and H3K4me1/3 by ChIP in mouse ES cells. Precipitation of formaldehyde cross-linked chromatin prepared from mouse ES cell using specific antibodies against Histone H3 and its specific modifications. Rabbit IgG were used as control.

2013-12-05 | E-GEOD-39496 | biostudies-arrayexpress

Polycomb-dependent H3K27me1 and H3K27me2 characterization in mouse ES cells (E14 and E36 with H3K27me1/2 and H3)

Project description:These data include the genome wide location analysis of H3K27me1/2/ac and H3K4me1/3 by ChIP in mouse ES cells.

2013-12-11 | GSE40109 | GEO

Polycomb-dependent H3K27me1 and H3K27me2 characterization in mouse ES cells (E36 with H3K27ac, H3K27me1, and H3K4me1/3)

Project description:These data include the genome wide location analysis of H3K27me1/2/ac and H3K4me1/3 by ChIP in mouse ES cells.

2013-12-05 | GSE39496 | GEO

Polycomb-dependent H3K27me1 and H3K27me2 characterization in mouse ES cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-12-05 | E-GEOD-40118 | biostudies-arrayexpress

Polycomb-dependent H3K27me1 and H3K27me2 regulate active transcription and enhancer fidelity

Project description:These data include the genome wide location of different histone modifications by ChIP sequencing in mouse ES cells, and RNA Seq data generated from wild type and EED KO mouse ES cells and knocked down for unrelated protein and Setd2 protein. ChIP-Seq: Immuno-precipitation of formaldehyde cross-linked chromatin prepared from wild type mouse E14 ES cells, wild type E36 ES cells, EED KO E36 ES cells, wild type Embryoid bodies (Ebs), EED KO Embryoid bodies (Ebs EED KO) using specific antibody against different histone modifications. RNA-Seq: Total RNA extracted from wild type E36 ES cells, EED KO E36 ES cells, wild type E36 Embryoid bodies (Ebs), EED KO Embryoid bodies (Ebs EED KO), E14 Ctrl KD, E14 Setd2 KD.

2013-12-05 | E-GEOD-51006 | biostudies-arrayexpress

Ogt chromatin recruitment is mediated by TET proteins in mouse ES cells [ChIP-Seq]

Project description:These data include the genome wide location analysis of Ogt by ChIP of Ogt in mouse ES cells. Precipitation of formaldehyde cross-linked chromatin prepared from mouse ES cell using specific antibody against OGT and IgG as control.

2013-01-06 | E-GEOD-39154 | biostudies-arrayexpress

Polycomb-dependent H3K27me1 and H3K27me2 regulate active transcription and enhancer fidelity

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Yy1 occupancy of mouse ES cell genome

Project description:These data include the genome wide location analyses of Yy1 by bioChIPs of Fbio-Yy1. Streptavidin precipitation of formaldehyde cross-linked chromatin prepared from Fbio-Yy1 and control expressing mouse ES cells

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Essential and unexpected role of YY1 to promote mesodermal cardiac differentiation

Project description:Rationale: Cardiogenesis is regulated by a complex interplay between transcription factors and chromatin-modifying enzymes. However, little is known about how these interactions regulate the transition from mesodermal precursors to cardiac progenitor cells (CPCs). Objective: To identify novel regulators of mesodermal cardiac lineage commitment. Methods and Results: We performed a bioinformatic-based transcription factor-binding site analysis on upstream promoter regions of genes that are enriched in ES cell-derived CPCs. From 32 candidate transcription factors screened, we found that YY1, a repressor of sarcomeric gene expression, is present in CPCs in vivo. Interestingly, we uncovered the ability of YY1 to transcriptionally activate Nkx2.5, a key marker of early cardiogenic commitment. YY1 regulates Nkx2.5 expression via a 2.1 kb cardiac-specific enhancer as demonstrated by in vitro luciferase-based assays and in vivo chromatin immunoprecipitation (ChIP) and genome-wide sequencing analysis. Furthermore, the ability of YY1 to activate Nkx2.5 expression depends on its cooperative interaction with GATA4 at a nearby chromatin. Cardiac mesoderm-specific loss-of-function of YY1 resulted in early embryonic lethality. This was corroborated in vitro by ES cell-based assays where we show that the over-expression of YY1 enhanced the cardiogenic differentiation ES cells into CPCs in a cell autonomous manner. Conclusion: These results demonstrate an essential and unexpected role for YY1 to promote cardiogenesis as a transcriptional activator of Nkx2.5 and other CPC-enriched genes. We report the identification of putative YY1 target genes in cardiac progenitor cells (CPCs). Two samples of independently FACS-purified eGFP+ CPCs were examined against the input.

2013-06-01 | E-GEOD-35370 | biostudies-arrayexpress

Genome-wide maps of chromatin state in wild-type and SetDB1 induced knockout mESCs

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells and characterized genome-wide SetDB1 binding and H3K9 trimethylation (H3K9me3) profiles in mouse ES cells and uncovered two distinct classes of SetDB1 binding sites, termed solo and ensemble peaks. The solo peaks were devoid of H3K9me3 and enriched near developmental regulators while the ensemble peaks were associated with H3K9me3. A subset of the SetDB1 solo peaks, particularly those near neural development related genes, was found to be associated with Polycomb Repressive Complex 2 (PRC2) as well as PRC2-interacting proteins Jarid2 and Mtf2. Genetic deletion of Setdb1 dramatically reduced Ezh2 binding as well as histone 3 lysine 27 (H3K27) trimethylation level at SetDB1 solo peaks and facilitated neural differentiation. Furthermore, we found that H3K27me3 inhibits SetDB1 methyltransferase activity in vitro. The currently identified reciprocal action between SetDB1 and PRC2 reveals a novel mechanism underlying ES cell pluripotency and differentiation regulation. Examination of 2 different histone modifications in 2 cell status.

2015-06-25 | E-GEOD-62666 | biostudies-arrayexpress

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