期刊
MOLECULAR CELL
卷 38, 期 3, 页码 452-464出版社
CELL PRESS
DOI: 10.1016/j.molcel.2010.02.032
关键词
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资金
- Medical Research Council [G0800784B, G0800784, G0300723B, MC_U127527202] Funding Source: researchfish
- MRC [G0800784, MC_U127527202] Funding Source: UKRI
- Medical Research Council [G0800784, MC_U127527202] Funding Source: Medline
- NCI NIH HHS [R01 CA079057, R01 CA079057-13, CA79057, R56 CA079057] Funding Source: Medline
- Wellcome Trust [087530] Funding Source: Medline
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 Ring 1B null cells that still have PRC2mediated 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.
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