SAM domain polymerization links subnuclear clustering of PRC1 to gene silencing.
Dev Cell, 2013/9/30;26(6):565-77.
Isono K[1], Endo TA, Ku M, Yamada D, Suzuki R, Sharif J, Ishikura T, Toyoda T, Bernstein BE, Koseki H
Affiliations
PMID: 24091011
Impact factor: 13.417
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.
MeSH terms
Animals; Cell Line; Cell Nucleus; Chromatin; Cytoplasm; Epigenetic Repression; Fibroblasts; Gene Silencing; Mice; Polycomb Repressive Complex 2; Polycomb-Group Proteins; Protein Binding; Protein Multimerization; Protein Structure, Tertiary; Transcription, Genetic
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