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Cell-type specific control of enhancer activity by H3K9 trimethylation

ABSTRACT: Cell-type specific control of enhancer activity by H3K9 trimethylation

PROVIDER: PRJNA147957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR349978.fastq.gz	Fastqsanger.gz
	SRR349979.fastq.gz	Fastqsanger.gz
	SRR349980.fastq.gz	Fastqsanger.gz
	SRR349981.fastq.gz	Fastqsanger.gz
	SRR349982.fastq.gz	Fastqsanger.gz

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Cell-type specific control of enhancer activity by H3K9 trimethylation

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2012-05-27 | E-GEOD-32381 | biostudies-arrayexpress

Cell-type specific control of enhancer activity by H3K9 trimethylation

Project description:This SuperSeries is composed of the SubSeries listed below.

2012-05-28 | GSE32381 | GEO

Genome-wide profiling of H3K9/K14 Acetylation and H3K27 trimethylation at promoters in the human lung embryonic fibroblast cell line MRC5

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Activity of a stem cell enhancer influences stem cell programs and clinical outcome in leukaemia

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Project description:The transcription factor MYC is overexpressed in most cancers, where it drives multiple hallmarks of cancer progression. MYC is known to promote oncogenic transcription by binding to active promoters. In addition, MYC has also been shown to invade distal enhancers when expressed at oncogenic levels, but this enhancer binding has been proposed to have low gene-regulatory potential. Here, we demonstrate that MYC enhancer binding directly promotes cancer type-specific gene programs predictive of poor patient prognosis. MYC induces transcription of enhancer RNA through recruitment of RNAPII, rather than regulating RNAPII pause-release as is the case at promoters. This is mediated by MYC-induced H3K9 demethylation by KDM3A and acetylation by GCN5, leading to enhancer-specific BRD4 recruitment through its bromodomains, which facilitates RNAPII recruitment. Thus, we propose that MYC drives prognostic cancer type-specific gene programs by promoting RNAPII recruitment to enhancers through induction of an epigenetic switch.

2023-11-30 | PXD039586 | Pride

Mechanism suppressing H3K9 trimethylation in pluripotent stem cells and its demise by polyQ-expanded huntingtin mutations [ChIP-seq]

Project description:We find that HTT binds ATF7IP, a regulator of the histone H3 methyltransferase SETDB1. HTT inhibits the interaction of the ATF7IP-SETDB1 complex with other heterochromatin regulators and transcriptional repressors, maintaining low levels of H3K9 trimethylation (H3K9me3) in hESCs. Conversely, loss of HTT promotes global increased H3K9me3 levels. To test whether HTT knockdown also induces enrichment of H3K9me3 marks at specific genes, we performed chromatin immunoprecipitation (ChIP)-sequencing assays of hESCs using an antibody to H3K9me3.

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Mechanism suppressing H3K9 trimethylation in pluripotent stem cells and its demise by polyQ-expanded huntingtin mutations [RNA-seq]

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Project description:Forkhead Box O (FOXO) transcription factors are versatile players in diverse cellular processes, affecting tumorigenesis, metabolism, stem cell maintenance and lifespan. To understand the transcriptional output of FOXO3 activation, we investigate features that define the subset of enhancer binding events that actually contribute to gene regulation. We show FOXO3 transcriptional output is determined by the amount of bound FOXO3, which in turn is determined by motif presence, pre-existing enhancer activity and accessibility. In this manner, FOXO3 amplifies pre-existing levels of activity marks and potentiates enhancer RNA transcription. We conclude that not only enhancer presence and sequence content, but also the pre-existing activity dictates FOXO3 binding and transcriptional output. Considering the flexible and cell type specific nature of regulatory regions and their activity, our observations provide a novel explanation for the diversity in FOXO transcriptional programs and introduce chromatin context as a new player in the regulation of FOXO activity in ageing and disease. Examination of histone modifications and transcriptome changes upon FOXO activation

2013-11-26 | E-GEOD-50243 | biostudies-arrayexpress

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