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Ezh1 and Ezh2 Maintain Repressive Chromatin through Different Mechanisms

Open access
Margueron, Raphael, Li, Guohong, Sarma, Kavitha, Blais, Alexandre, Zavadil, Jiri, Woodcock, Christopher L., Dynlacht, Brian D., Reinberg, Danny·2008·Molecular Cell

Abstract

Polycomb group proteins are critical to maintaining gene repression established during Drosophila development. Part of this group forms the PRC2 complex containing Ez that catalyzes methylation of histone H3 lysine 27 (H3K37me2/3), marks repressive to transcription. We report that the mammalian homologs Ezh1 and Ezh2 form similar PRC2 complexes but exhibit contrasting repressive roles. While PRC2-Ezh2 catalyzes H3K27me2/3 and its knockdown affects global H3K27me2/3 levels, PRC2-Ezh1 performs this function weakly. In accordance, Ezh1 knockdown was ineffectual on global H3K27me2/3 levels. Instead, PRC2-Ezh1 directly and robustly represses transcription from chromatinized templates and compacts chromatin in the absence of the methyltransferase cofactor SAM, as evidenced by electron microscopy. Ezh1 targets a subset of Ezh2 genes, yet Ezh1 is more abundant in non-proliferative adult organs while Ezh2 expression is tightly associated with proliferation as evidenced when analyzing aging mouse kidney. These results might reflect sub-functionalization of a PcG protein during evolution.

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Metadata

Authors
Margueron, R., Li, G., Sarma, K., Blais, A., Zavadil, J., Woodcock, C. L., Dynlacht, B. D., & Reinberg, D.
Venue
Molecular Cell
Publisher
Elsevier BV
Published
2008-11
Volume
32
Issue
4
Pages
503-518
ISSN
1097-2765 (ISSN-L)
OpenAlex
W2025856640
Cited by
884
References
4
FWCI
12.90
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Ezh1 and Ezh2 Maintain Repressive Chromatin through Different Mechanisms. https://app.cochat.ai/papers/10.1016/j.molcel.2008.11.004
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Margueron, R., Li, G., Sarma, K., Blais, A., Zavadil, J., Woodcock, C. L., Dynlacht, B. D., & Reinberg, D. (2008). Ezh1 and Ezh2 Maintain Repressive Chromatin through Different Mechanisms. Molecular Cell. https://doi.org/10.1016/j.molcel.2008.11.004

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