Ring1B compacts chromatin structure and represses gene expression independent of histone ubiquitination.
How polycomb group proteins repress gene expression in vivo is not known. While histone-modifying activities of the polycomb repressive complexes (PRCs) have been studied extensively, in vitro data have suggested a direct activity of the PRC1 complex in compacting chromatin. Here, we investigate higher-order chromatin compaction of polycomb targets in ... vivo. We show that PRCs are required to maintain a compact chromatin state at Hox loci in embryonic stem cells (ESCs). There is specific decompaction in the absence of PRC2 or PRC1. This is due to a PRC1-like complex, since decompaction occurs in Ring1B null cells that still have PRC2-mediated H3K27 methylation. Moreover, we show that the ability of Ring1B to restore a compact chromatin state and to repress Hox gene expression is not dependent on its histone ubiquitination activity. We suggest that Ring1B-mediated chromatin compaction acts to directly limit transcription in vivo.
Mesh Terms:
Acetylation, Animals, Cell Differentiation, Cell Line, Chromatin Assembly and Disassembly, Down-Regulation, Embryonic Stem Cells, Histones, Homeodomain Proteins, Methylation, Mice, Mutation, Protein Processing, Post-Translational, Repressor Proteins, Transcription, Genetic, Ubiquitination
Acetylation, Animals, Cell Differentiation, Cell Line, Chromatin Assembly and Disassembly, Down-Regulation, Embryonic Stem Cells, Histones, Homeodomain Proteins, Methylation, Mice, Mutation, Protein Processing, Post-Translational, Repressor Proteins, Transcription, Genetic, Ubiquitination
Mol. Cell
Date: May. 14, 2010
PubMed ID: 20471950
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