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Polycomb repressive complex 1 defines the nucleosome landscape but not accessibility at target genes

ABSTRACT: Polycomb repressive complex 1 defines the nucleosome landscape but not accessibility at target genes

PROVIDER: PRJNA384999 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5488980_1.fastq.gz	Fastqsanger.gz
	SRR5488980_2.fastq.gz	Fastqsanger.gz
	SRR5488990_1.fastq.gz	Fastqsanger.gz
	SRR5488990_2.fastq.gz	Fastqsanger.gz
	SRR5489000_1.fastq.gz	Fastqsanger.gz

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Polycomb repressive complex 1 regulates the nucleosome landscape but not accessibility at target genes [RNA-seq]

Project description:Polycomb repressive complexes 1 and 2 (PRC1/2) act to limit transcriptional activity at gene promoters. One of the mechanisms by which they are proposed to achieve this is through the compaction of nucleosomal chromatin. However, this model is based largely upon in vitro studies and has yet to be explored sufficiently in living cells. We therefore characterised the chromatin accessibility of Polycomb-occupied gene promoters using assay for transposase accessible chromatin (ATAC-seq). Although Polycomb-occupied promoters exist in a less accessible state compared to Polycomb-free promoters, we were surprised to observe that deletion of either PRC1, PRC2 or both PRC1/2 did not result in any increases in chromatin accessibility. This was in contrast to widespread increases in the transcriptional activity of Polycomb target genes. Together with experiments examining chromatin accessibility in the context of RNA polymerase II inhibition, we therefore demonstrate an apparent uncoupling of the chromatin accessibility and transcriptional activity of gene promoters.

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Polycomb repressive complex 1 regulates the nucleosome landscape but not accessibility at target genes [ATAC-seq]

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Polycomb repressive complex 1 shapes the nucleosome landscape but not accessibility at target genes.

Project description:Polycomb group (PcG) proteins are transcriptional repressors that play important roles in regulating gene expression during animal development. In vitro experiments have shown that PcG protein complexes can compact chromatin to limit the activity of chromatin remodeling enzymes and access of the transcriptional machinery to DNA. In fitting with these ideas, gene promoters associated with PcG proteins have been reported to be less accessible than other gene promoters. However, it remains largely untested in vivo whether PcG proteins define chromatin accessibility or other chromatin features. To address this important question, we examine the chromatin accessibility and nucleosome landscape at PcG protein-bound promoters in mouse embryonic stem cells using the assay for transposase accessible chromatin (ATAC)-seq. Combined with genetic ablation strategies, we unexpectedly discover that although PcG protein-occupied gene promoters exhibit reduced accessibility, this does not rely on PcG proteins. Instead, the Polycomb repressive complex 1 (PRC1) appears to play a unique role in driving elevated nucleosome occupancy and decreased nucleosomal spacing in Polycomb chromatin domains. Our new genome-scale observations argue, in contrast to the prevailing view, that PcG proteins do not significantly affect chromatin accessibility and highlight an underappreciated complexity in the relationship between chromatin accessibility, the nucleosome landscape, and PcG-mediated transcriptional repression.

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Project description:LATS2 regulates repressive epigenetic integrity via regulation of Polycomb repressive complex 2

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Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors

Project description:This SuperSeries is composed of the following subset Series: GSE33653: Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors (ChIP-Seq) GSE33659: Direct Recruitment of Polycomb Repressive Complex 1 (PRC1) to Chromatin by Core Binding Transcription Factors (microarray) Refer to individual Series

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Project description:Nucleation and spreading of H3K27me3 are critical steps for the initiation and maintenance, respectively, of mitotically inheritable Polycomb-mediated repressive chromatin states in cell identity memory, in both animals and plants. Although a semiconservative read-and-write mechanism is proposed to play a key role in H3K27me3 propagation, the specific determinant and underlying mechanism by which the Polycomb Repressive Complex 2 (PRC2) accesses unmodified nucleosomes for propagating H3K27me3 remain enigmatic. Using Arabidopsis thaliana as a model, we show that the chromatin remodeling activity of PICKLE (PKL) has a specialized role in H3K27me3 spreading to safeguard cell identity during differentiation. PKL specifically binds to H3K27me3 spreading regions but not nucleation sites of Polycomb target genes and physically interacts with the MSI1 subunit of PRC2. Loss of PKL abolishes the occupancy of the PRC2 catalytic subunit CLF in spreading regions and leads to aberrant differentiation. Nucleosome condensing endowed by the ATPase function of PKL ensures that unmodified nucleosomes are accessible to PRC2 catalytic activity. Our findings highlight that PKL-dependent nucleosome compaction is critical for PRC2-mediated H3K27me3 read-and-write functions in H3K27me3 spreading, thus revealing a mechanism by which repressive chromatin domains are established and propagated.

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Polycomb repressive complex 1 defines the nucleosome landscape but not accessibility at target genes

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

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Project description:Polycomb Repressive Complexes 1 and 2 (PRC1, PRC2) are conserved epigenetic regulators that promote transcriptional silencing. PRC1 and PRC2 converge on shared targets, catalyzing repressive histone modifications. In addition, a subset of PRC1/PRC2 targets engage in long-range interactions whose functions in gene silencing are poorly understood. Using a CRISPR screen in mouse embryonic stem cells, we discovered that the cohesin regulator PDS5A links transcriptional silencing by Polycomb and 3D genome organization. PDS5A deletion impairs cohesin unloading and results in derepression of subset of endogenous PRC1/PRC2 target genes. Importantly, derepression is not associated with loss of repressive Polycomb chromatin modifications. Instead, loss of PDS5A leads to aberrant cohesin activity, ectopic insulation sites and specific reduction of ultra-long Polycomb loops. We infer that these loops are important for robust silencing at a subset of Polycomb target genes and that maintenance of cohesin-dependent genome architecture is critical for Polycomb regulation.

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