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Nucleic Acids Res. 2016 Dec 1;44(21):10132-10149. Epub 2016 Aug 23.

Interdependence of PRC1 and PRC2 for recruitment to Polycomb Response Elements.

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Department of Molecular Biology, Umeå University, Umeå, 901 87, Sweden.
Friedrich-Alexander University of Erlangen-Nürnberg, Department of Biology, Division of Developmental Biology, Erlangen, D-91058, Germany.
Division of CBRN Defense and Security, Swedish Defense Research Agency, FOI, Umeå, 906 21, Sweden.
Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ 08854, USA.
Department of Molecular Biology, Umeå University, Umeå, 901 87, Sweden


Polycomb Group (PcG) proteins are epigenetic repressors essential for control of development and cell differentiation. They form multiple complexes of which PRC1 and PRC2 are evolutionary conserved and obligatory for repression. The targeting of PRC1 and PRC2 is poorly understood and was proposed to be hierarchical and involve tri-methylation of histone H3 (H3K27me3) and/or monoubiquitylation of histone H2A (H2AK118ub). Here, we present a strict test of this hypothesis using the Drosophila model. We discover that neither H3K27me3 nor H2AK118ub is required for targeting PRC complexes to Polycomb Response Elements (PREs). We find that PRC1 can bind PREs in the absence of PRC2 but at many PREs PRC2 requires PRC1 to be targeted. We show that one role of H3K27me3 is to allow PcG complexes anchored at PREs to interact with surrounding chromatin. In contrast, the bulk of H2AK118ub is unrelated to PcG repression. These findings radically change our view of how PcG repression is targeted and suggest that PRC1 and PRC2 can communicate independently of histone modifications.

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