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Specialized replication of heterochromatin domains ensures self-templated chromatin assembly and epigenetic inheritance [ChIP-chip H3K9me3]

ABSTRACT: Occupancy profiling of lysine 9 trimethylated histone H3 in fission yeast.

ORGANISM(S): Schizosaccharomyces pombe

PROVIDER: GSE242429 | GEO | 2024/02/02

REPOSITORIES: GEO

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Specialized replication of heterochromatin domains ensures self-templated chromatin assembly and epigenetic inheritance

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Trithorax-group protein ASH1 defines novel H3K36me3/H3K9me3 bivalent domains

Project description:A Trithorax-group (TrxG) protein ASH1 selectively dimethylates histone H3 lysine 36 (H3K36) and is required for expression of Hox genes. Genome-wide targets and molecular functions of ASH1, however, have remained elusive. Here we report ChIP-seq analysis of ASH1 targets in the human genome using a leukemia cell line K562. We identified 4,596 ASH1 binding sites, 2,502 of which are in the coding region, mostly in a proximity of promoters. Remaining half of the ASH1 binding sites are in the intergenic region. Analysis of histone methyation patterns revealed that a majority of ASH1 bidning sites are closely associated not only with trimethylated H3K36 (H3K36me3) but also with H3K9me3, shedding light for the first time to H3K36/H3K9 double methylation domains. Of note, an H3K9 methyltransferase SETDB1 is enriched in the ASH1 bidning sites, whereas EZH2 but not SUZ12 of the Polycomb Repression Complex 2 (PRC2) is present in bivalent domains. In addition, a small subset of ASH1 targets bear H3K4me3 and colocalize with RNA polymerase II. These select targets are highly enriched for regulators of gene expression, such as CXXC1, WHSC2/NELFA, and a battery of zinc finger proteins, suggesting that ASH1 might acts as a master regulator of gene expression.

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Project description:Mono-methylation of lysine 4 on histone H3 (H3K4me1) is a well-established feature of enhancers and promoters, although its function is unknown. Remarkably, we find H3K4me1 at the promoter regions of conditionaly-repressed muscle and stimulus-dependent inflammatory response genes in myoblasts. During myogenesis, muscle genes are activated and become H3K4-trimethylated. On the promoters of active genes, we find that H3K4me1 spatially restricts the recruitment of “readers” of H3K4me3, including ING1, which, in turn, recruits Sin3A. Our findings point to a unique role for H3K4 mono-methylation in establishing boundaries that restrict the recruitment of chromatin-modifying enzymes to defined regions within promoters. Mapping of Wdr5, Menin, MLL1, Sin3A, and LSD1 in growing myoblasts (MB) and ING1 in growing myoblasts (MB) and fully differentiated myotubes (MT).

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