The Polycomb group protein EZH2 directly controls DNA methylation

Emmanuelle Viré, Carmen Brenner, Rachel Deplus, Loïc Blanchon, Mario Fraga, Céline Didelot, Lluis Morey, Aleyde Van Eynde, David Bernard, Jean-Marie Vanderwinden, Mathieu Bollen, Manel Esteller, Luciano Di Croce, Yvan de Launoit and François Fuks ()
Additional contact information
Emmanuelle Viré: Free University of Brussels
Carmen Brenner: Free University of Brussels
Rachel Deplus: Free University of Brussels
Loïc Blanchon: Free University of Brussels
Mario Fraga: CNIO, Cancer Epigenetics Group
Céline Didelot: Free University of Brussels
Lluis Morey: ICREA and CRG
Aleyde Van Eynde: Katholieke Universiteit Leuven
David Bernard: Free University of Brussels
Jean-Marie Vanderwinden: Free University of Brussels
Mathieu Bollen: Katholieke Universiteit Leuven
Manel Esteller: CNIO, Cancer Epigenetics Group
Luciano Di Croce: ICREA and CRG
Yvan de Launoit: Free University of Brussels
François Fuks: Free University of Brussels

Nature, 2006, vol. 439, issue 7078, 871-874

Abstract: Abstract The establishment and maintenance of epigenetic gene silencing is fundamental to cell determination and function1. The essential epigenetic systems involved in heritable repression of gene activity are the Polycomb group (PcG) proteins2,3 and the DNA methylation4,5 systems. Here we show that the corresponding silencing pathways are mechanistically linked. We find that the PcG protein EZH2 (Enhancer of Zeste homolog 2) interacts—within the context of the Polycomb repressive complexes 2 and 3 (PRC2/3)—with DNA methyltransferases (DNMTs) and associates with DNMT activity in vivo. Chromatin immunoprecipitations indicate that binding of DNMTs to several EZH2-repressed genes depends on the presence of EZH2. Furthermore, we show by bisulphite genomic sequencing that EZH2 is required for DNA methylation of EZH2-target promoters. Our results suggest that EZH2 serves as a recruitment platform for DNA methyltransferases, thus highlighting a previously unrecognized direct connection between two key epigenetic repression systems.

Date: 2006
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DOI: 10.1038/nature04431

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