4.8 Article

p300/CBP sustains Polycomb silencing by non-enzymatic functions

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MOLECULAR CELL
卷 82, 期 19, 页码 3580-+

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CELL PRESS
DOI: 10.1016/j.molcel.2022.09.005

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  1. Swedish Cancer Society (Cancerfonden)
  2. Swedish Research Council (Vetenskapsradet)

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Maintenance of appropriate cell states involves epigenetic mechanisms, including Polycomb-group (PcG)-mediated transcriptional repression. This study reveals the association between the p300/CREB-binding protein (CBP) co-activator and PcG regions in Drosophila and mouse cells. CBP stabilizes Pol II at PcG-bound repressive sites and promotes Pol II pausing, which are necessary for R-loop formation and nucleosome depletion at Polycomb Response Elements (PREs), thereby supporting PcG-mediated silencing.
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/CREB-binding protein (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 re-gion is not. These results suggest that non-enzymatic activities of the CBP co-activator have been repur-posed to support PcG-mediated silencing, revealing how chromatin regulator interplay maintains transcriptional states.

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