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H3K4me2/3 modulate the stability of RNA polymerase II pausing (ChIP-Seq)

ABSTRACT: H3K4me2/3 modulate the stability of RNA polymerase II pausing (ChIP-Seq)

PROVIDER: PRJNA923650 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23075400_1.fastq.gz	Fastqsanger.gz
	SRR23075400_2.fastq.gz	Fastqsanger.gz
	SRR23075401_1.fastq.gz	Fastqsanger.gz
	SRR23075401_2.fastq.gz	Fastqsanger.gz
	SRR23075402_1.fastq.gz	Fastqsanger.gz

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H3K4me2/3 modulate the stability of RNA polymerase II pausing

Project description:H3K4me2/3 modulate the stability of RNA polymerase II pausing

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H3K4me2/3 modulate the stability of RNA polymerase II pausing (PRO-Seq)

Project description:H3K4me2/3 modulate the stability of RNA polymerase II pausing (PRO-Seq)

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H3K4me2/3 modulate the stability of RNA polymerase II pausing (RNA-Seq)

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H3K4me2/3 modulate the stability of RNA polymerase II pausing (RNA-Seq)

Project description:Modifications of histones are intricately linked with the regulation of gene expression, with demonstrated roles in various physiological processes and disease pathogenesis. Methylation of histone H3 lysine 4 (H3K4), implemented by the COMPASS family, is enriched at promoters and associated cis-regulatory elements, with H3K4 trimethylation (H3K4me3) considered a hallmark of active gene promoters. However, the relative roles of deposition and removal of H3K4 methylation, as well as the extent to which these events contribute to transcriptional regulation have so far remained unclear. Here, through rapid depletion of either of two shared subunits of COMPASS family members, we reveal a dynamic turnover of H3K4me2 and H3K4me3 mediated by the KDM5 family of histone demethylases. Loss of H3K4me2 and H3K4me3 following COMPASS disruption does not impair the recruitment of TFIID and initiating RNA polymerase II (Pol II). Instead, their loss leads to reductions in the paused form of Pol II on chromatin while inducing the relative enrichment of the Integrator-PP2A (INTAC) termination complex, leading to reduced levels of elongating polymerases, thus revealing how H3K4me2 and H3K4me3 dynamics can regulate Pol II pausing to sustain or attenuate transcription.

2023-03-18 | GSE222847 | GEO

H3K4me2/3 modulate the stability of RNA polymerase II pausing (PRO-Seq)

2023-03-18 | GSE222846 | GEO

H3K4me2/3 modulate the stability of RNA polymerase II pausing (ChIP-Seq)

2023-03-18 | GSE222845 | GEO

H3K4me2/3 modulate the stability of RNA polymerase II pausing.

Project description: Not available

| S-EPMC10156655 | biostudies-literature

H3K4me2/3 modulate the stability of RNA polymerase II pausing

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

2023-03-18 | GSE222848 | GEO

Reporter-ChIP-nexus reveals strong contribution of the Drosophila initiator sequence to RNA polymerase pausing

Project description:RNA polymerase II (Pol II) pausing is a general regulatory step in transcription, yet the stability of paused Pol II varies widely between genes. Although paused Pol II stability correlates with core promoter elements, the contribution of individual sequences remains unclear, in part because no rapid assay is available for measuring the changes in Pol II pausing as a result of altered promoter sequences. Here, we overcome this hurdle by showing that ChIP-nexus captures the endogenous Pol II pausing on transfected plasmids. Using this reporter-ChIP-nexus assay in Drosophila cells, we show that the pausing stability is influenced by downstream promoter sequences, but that the strongest contribution to Pol II pausing comes from the initiator sequence, in which a single nucleotide, a G at the +2 position, is critical for stable Pol II pausing. These results establish reporter-ChIP-nexus as a valuable tool to analyze Pol II pausing.

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Reduced polymerase pausing compensates for increased chromatin accessibility in the aging liver

Project description:Regulation of gene expression is linked to the organization of the genome. With age, chromatin alterations occur on all levels of genome organization, accompanied by changes in the gene expression profile. However, little is known about the changes on the level of transcriptional regulation. Here, we used a multi-omics approach and integrated ATAC-, RNA- and NET-seq to identify age-related changes in the chromatin landscape of murine liver and to investigate how these are linked to transcriptional regulation. We provide the first systematic inventory of the connection between aging, chromatin accessibility and transcriptional regulation in a whole tissue. Aging in murine liver is characterized by an increase in chromatin accessibility at promoter regions, but not in an increase of transcriptional output. Instead, aging is accompanied by a decrease of promoter-proximal pausing of RNA polymerase II (Pol II). We propose that these changes in transcriptional regulation are due to a reduced stability of the pausing complex and may represent a mechanism to compensate for the age-related increase in chromatin accessibility in order to prevent aberrant transcription.

2022-09-15 | PXD034564 | Pride

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