A role for mammalian Sin3 in permanent gene silencing.
A role for mammalian Sin3 in permanent gene silencing.
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DOI：
10.1016/j.molcel.2008.10.015
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发表时间：
2008-11-07
期刊：
影响因子：
16
通讯作者：
Dynlacht, Brian David
中科院分区：
文献类型：
--
作者：
van Oevelen, Chris;Wang, Jinhua;Asp, Patrik;Yan, Qin;Kaelin, William G., Jr.;Kluger, Yuval;Dynlacht, Brian David
The multi-subunit Sin3 co-repressor complex regulates gene transcription through deacetylation of nucleosomes. However, the full range of Sin3 activities and targets is not well understood. Here, we have investigated genome-wide binding of mouse Sin3 and RBP2 as well as histone modifications and nucleosome positioning as a function of myogenic differentiation. Remarkably, we find that Sin3 complexes spread immediately downstream of the transcription start site on repressed and transcribed genes during differentiation. We show that RBP2 is part of a Sin3 complex, and on a subset of E2F4 target genes, the coordinated activity of Sin3 and RBP2 leads to deacetylation, demethylation, and repositioning of nucleosomes. Our work provides evidence for coordinated binding of Sin3, chromatin modifications, and chromatin remodeling within discrete regulatory regions, suggesting a model in which spreading of Sin3 binding is ultimately linked to permanent gene silencing on a subset of E2F4 target genes.
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