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P300/CBP sustains Polycomb silencing by non-enzymatic functions (ChIP-seq on inhibitor-treated Drosophila S2 cells)

ABSTRACT: p300/CBP sustains Polycomb silencing by non-enzymatic functions (ChIP-seq on inhibitor-treated Drosophila S2 cells)

PROVIDER: PRJNA725709 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14341200.fastq.gz	Fastqsanger.gz
	SRR14341201.fastq.gz	Fastqsanger.gz
	SRR14341202.fastq.gz	Fastqsanger.gz
	SRR14341203.fastq.gz	Fastqsanger.gz
	SRR14341204.fastq.gz	Fastqsanger.gz

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p300/CBP sustains Polycomb silencing by non-enzymatic functions

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p300/CBP sustains Polycomb silencing by non-enzymatic functions (ChIP-seq on RNAi-treated Drosophila S2 cells)

Project description:Maintenance of appropriate cell states involves epigenetic mechanisms, including Polycomb group (PcG)-mediated transcriptional repression. While PcG proteins are known to induce chromatin compaction, how PcG proteins gain access to DNA in compact chromatin to achieve long-term silencing is poorly understood. Here we show that the p300/CBP co-activator is associated with two-thirds of PcG-regions and required for PcG occupancy at many of these in Drosophila and mouse cells. CBP stabilizes RNA polymerase II (Pol II) at PcG-bound repressive sites and promotes Pol II pausing independently of its histone acetyltransferase activity. CBP and Pol II pausing are necessary for RNA-DNA hybrid (R-loop) formation and nucleosome depletion at Polycomb Response Elements (PREs), whereas transcription beyond the pause region is not. These results suggest that non-enzymatic activities of the CBP co-activator have been repurposed to support PcG-mediated silencing, revealing how chromatin regulator interplay maintains transcriptional states.

2022-10-06 | GSE186721 | GEO