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Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them.

ABSTRACT: We found that CTCF sites was acetylated at H3K27 and this modification was decreased by histone acetyltransferases and depletion of GATA-1.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146827 | GEO | 2021/03/12

REPOSITORIES: GEO

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Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them

Project description:We found that H3K27ac at CTCF sites was decreased around the β-globin locus by loss of GATA-1 binding.

2021-03-15 | GSE147037 | GEO

Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them.

Project description:Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them.

| PRJNA612057 | ENA

Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them

Project description:Histone H3K27 acetylation at CTCF sites mediates cell type-specific chromatin interactions between them

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DUX4 recruits p300/CBP through its C-terminus and induces global H3K27 acetylation changes

Project description:Ectopic expression of the double homeodomain transcription factor DUX4 causes facioscapulohumeral muscular dystrophy (FSHD). Mechanisms of action of DUX4 are currently unknown. Using immortalized human myoblasts with a titratable DUX4 transgene, we identify by mass spectrometry an interaction between the DUX4 C-terminus and the histone acetyltransferases p300/CBP. Chromatin immunoprecipitation shows that DUX4 recruits p300 to its target gene, ZSCAN4, displaces histone H3 from the center of its binding site, and induces H3K27Ac in its vicinity, but C-terminal deleted DUX4 does not. We show that a DUX4 minigene, bearing only the homeodomains and C-terminus, is transcriptionally functional and cytotoxic, and that overexpression of a nuclear targeted C-terminus impairs the ability of WT DUX4 to interact with p300 and to regulate target genes. Genomic profiling of DUX4, histone H3, and H3 modifications reveals that DUX4 binds two classes of locus: DNase accessible H3K27Ac-rich chromatin and inaccessible H3K27Ac-depleted MaLR-enriched chromatin. At this latter class, it acts as a pioneer factor, recruiting H3K27 acetyltransferase activity and opening the locus for transcription. In concert with local increased H3K27Ac, the strong H3K27Ac peaks at distant sites are significantly depleted of H3K27Ac, thus DUX4 uses its C-terminus to induce a global reorganization of H3K27 acetylation. Two biological samples were analyzed with 4 antibodies for ChIP-Seq and in triplicate for RNA-Seq.

2016-03-10 | E-GEOD-78158 | biostudies-arrayexpress

Dissecting the Role of H3K27 Acetylation and Methylation in PRC2 Mediated Control of Cellular Identity

Project description:The Polycomb repressive complexes PRC1 and PRC2 act non-redundantly at target genes to maintain transcriptional programs and ensure cellular identity. PRC2 methylates lysine 27 on histone H3 (H3K27me), while PRC1 mono-ubiquitinates histone H2A at lysine 119 (H2Aub1). Here we present engineered mouse embryonic stem cells (ESCs) targeting the PRC2 subunits EZH1 and EZH2 to discriminate between contributions of distinct H3K27 methylation states and the presence of PRC2/1 at chromatin. We generate catalytically inactive EZH2 mutant ESCs, demonstrating that H3K27 methylation, but not recruitment to the chromatin, is essential for proper ESC differentiation. We further show that EZH1 activity is sufficient to maintain repression of Polycomb targets by depositing H3K27me2/3 and preserving PRC1 recruitment. This occurs in the presence of altered H3K27me1 deposition at actively transcribed genes and by a diffused hyperacetylation of chromatin that compromises ESC developmental potential. Overall, this work provides insights for the contribution of diffuse chromatin invasion by acetyltransferases in PRC2-dependent loss of developmental control.

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DUX4 recruits p300/CBP through its C-terminus and induces global H3K27 acetylation changes

2016-03-10 | GSE78158 | GEO

H3K27 acetylation and gene expression during late spermatogenesis

Project description:ChIP-seq for H3K27 acetylation and RNA-seq were performed during spermatogenesis. We analyzed two representative stages of spermatogenesis: purified pachytene spermatocytes (PS) undergoing meiosis; and postmeiotic round spermatids (RS) from adult testes.

2018-02-05 | GSE107398 | GEO

CBP/P300 Dependent Histone H3K27 Acetylation

Project description:Enhancer Activity Requires CBP/P300 Bromodomain Dependent Histone H3K27 Acetylation

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ChIP-seq of patient derived colorectal cancer cell lines using KLF5 and H3K27 acetylation

Project description:Discovery of genome-wide KLF5 binding sites in the PDCs. Chromatin was obtained from colorectal cancer cell line of one patient, and subjected to ChIP-seq using KLF5, H3K27 antibodies prepared using the NEB Next® ChIP-Seq Library kit (NEB Biolabs) according to the manufacturer’s instructions, and sequenced using the HiSeq 2000 system (Illumina). Raw data from input, KLF5 and H3K27 are uploaded.

2022-12-24 | E-MTAB-8080 | biostudies-arrayexpress

H3K27 Acetylation profile of hypothyroid NCoR1KO mice

Project description:We ablated the expression of the Nuclear Receptor Corepressor 1 specifically in mice livers and rendered them hypothyroid. Then we performed H3K27 acetylation CHIP-Seq. We found decreased H3K27ac in the livers of hypothyroid wild type and NCoR1KO mice. Therefore, we concluded that the thyroid hormone receptor may recruit histone deacetilases independently of NCoR1.

2017-09-18 | GSE99475 | GEO

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