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Mol Cell. 2014 Jan 23;53(2):277-89. doi: 10.1016/j.molcel.2013.12.005. Epub 2014 Jan 2.

The histone H3 lysine 9 methyltransferases G9a and GLP regulate polycomb repressive complex 2-mediated gene silencing.

Author information

1
Université Paris Diderot, Sorbonne Paris Cité, Laboratoire Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, 35 rue Hélène Brion, 75013 Paris, France. Electronic address: chiara.mozzetta@univ-paris-diderot.fr.
2
Université Paris Diderot, Sorbonne Paris Cité, Laboratoire Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, 35 rue Hélène Brion, 75013 Paris, France.
3
Institut Curie, 26 rue d'Ulm, 75005 Paris, France; UMR3215 CNRS, 26 rue d'Ulm, 75005 Paris, France; U934 INSERM, 26 rue d'Ulm, 75005 Paris, France.
4
Institut Pasteur, PF2 Plate-forme Transcriptome et Epigénome, 28 rue du Dr Roux, Paris, 75015 France.
5
Université Paris Diderot, Sorbonne Paris Cité, Laboratoire Epigénétique et Destin Cellulaire, UMR7216, Centre National de la Recherche Scientifique CNRS, 35 rue Hélène Brion, 75013 Paris, France. Electronic address: slimane.aitsiali@univ-paris-diderot.fr.

Abstract

G9a/GLP and Polycomb Repressive Complex 2 (PRC2) are two major epigenetic silencing machineries, which in particular methylate histone H3 on lysines 9 and 27 (H3K9 and H3K27), respectively. Although evidence of a crosstalk between H3K9 and H3K27 methylations has started to emerge, their actual interplay remains elusive. Here, we show that PRC2 and G9a/GLP interact physically and functionally. Moreover, combining different genome-wide approaches, we demonstrate that Ezh2 and G9a/GLP share an important number of common genomic targets, encoding developmental and neuronal regulators. Furthermore, we show that G9a enzymatic activity modulates PRC2 genomic recruitment to a subset of its target genes. Taken together, our findings demonstrate an unanticipated interplay between two main histone lysine methylation mechanisms, which cooperate to maintain silencing of a subset of developmental genes.

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PMID:
24389103
DOI:
10.1016/j.molcel.2013.12.005
[Indexed for MEDLINE]
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