期刊
CELL STEM CELL
卷 7, 期 1, 页码 114-126出版社
CELL PRESS
DOI: 10.1016/j.stem.2010.05.020
关键词
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资金
- Medical Research Council UK
- Leukaemia and Lymphoma Research
- EU [HPRN-CT 00504228]
- NIH [HD36720]
- Medical Research Council [MC_U120027516, MC_U120036884] Funding Source: researchfish
- MRC [MC_U120036884, MC_U120027516] Funding Source: UKRI
Modifications to the core histones are thought to contribute to ESC pluripotency by priming tissue-specific promoters and enhancers for later activation. However, it is unclear how these marks are targeted in ESCs and maintained during differentiation. Here, we show that the ESC factor Sox2 targets H3K4 methylation to monovalent and bivalent domains. In ESCs, Sox2 contributes to the formation of a monovalent mark at an enhancer in the pro/pre-B cell-specific lambda 5-VpreB1 locus. Binding of Foxd3 suppresses intergenic transcription of the enhancer and surrounding sequences. In pro-B cells, enhancer activity is dependent on the Sox and Fox binding sites, and the enhancer is bound by Sox4, which is required for efficient expression of lambda 5. Our results lead us to propose a factor relay model whereby ESC factors establish active epigenetic marks at tissue specific elements before being replaced by cell type-specific factors as cells differentiate.
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