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Dev Cell. 2013 Sep 30;26(6):565-77. doi: 10.1016/j.devcel.2013.08.016.

SAM domain polymerization links subnuclear clustering of PRC1 to gene silencing.

Author information

1
Laboratory for Developmental Genetics, RIKEN Center for Integrative Medical Sciences (IMS-RCAI), 1-7-22 Suehiro, Tsurumi-ku, Yokohama 230-0045, Japan; CREST, Japan Science and Technology Agency, 1-7-22 Suehiro, Tsurumi-ku, Yokohama 230-0045, Japan; PREST, Japan Science and Technology Agency, 1-7-22 Suehiro, Tsurumi-ku, Yokohama 230-0045, Japan. Electronic address: isono@rcai.riken.jp.

Abstract

The Polycomb-group (PcG) repressive complex-1 (PRC1) forms microscopically visible clusters in nuclei; however, the impact of this cluster formation on transcriptional regulation and the underlying mechanisms that regulate this process remain obscure. Here, we report that the sterile alpha motif (SAM) domain of a PRC1 core component Phc2 plays an essential role for PRC1 clustering through head-to-tail macromolecular polymerization, which is associated with stable target binding of PRC1/PRC2 and robust gene silencing activity. We propose a role for SAM domain polymerization in this repression by two distinct mechanisms: first, through capturing and/or retaining PRC1 at the PcG targets, and second, by strengthening the interactions between PRC1 and PRC2 to stabilize transcriptional repression. Our findings reveal a regulatory mechanism mediated by SAM domain polymerization for PcG-mediated repression of developmental loci that enables a robust yet reversible gene repression program during development.

PMID:
24091011
DOI:
10.1016/j.devcel.2013.08.016
[Indexed for MEDLINE]
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