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

ABSTRACT: 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.

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE186720 | GEO | 2022/10/06

REPOSITORIES: GEO

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p300/CBP sustains Polycomb silencing by non-enzymatic functions (ChIP-seq on inhibitor-treated mouse ES cells)

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