SAM domain polymerization links subnuclear clustering of PRC1 to gene silencing

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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. © 2013 Elsevier Inc.

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Isono, K., Endo, T. A., Ku, M., Yamada, D., Suzuki, R., Sharif, J., … Koseki, H. (2013). SAM domain polymerization links subnuclear clustering of PRC1 to gene silencing. Developmental Cell, 26(6), 565–577. https://doi.org/10.1016/j.devcel.2013.08.016

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