Journal
MOLECULAR CELL
Volume 53, Issue 2, Pages 277-289Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2013.12.005
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Funding
- Agence Nationale de la Recherche (H3K9-methylome grant)
- Agence Nationale de la Recherche (EPILIS grant)
- Association Francaise contre les Myopathies (AFM)
- Fondation Bettencourt-Schueller
- Fondation ARC
- GEFLUC
- Institut National du Cancer (INCa) [2012-1-PLBIO]
- CNRS
- Universite Paris Diderot
- FRM fellowship
- EMBO fellowship
- MESR
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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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