期刊
MOLECULAR CELL
卷 51, 期 3, 页码 310-325出版社
CELL PRESS
DOI: 10.1016/j.molcel.2013.07.010
关键词
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资金
- Fondation Leducq Career Development award
- Sigrid Juselius fellowship
- Academy of Finland
- ASLA-Fulbright
- Finnish Foundation for Cardiovascular Research
- Finnish Cultural Foundation (North Savo Regional Fund)
- Orion-Farmos Research Foundation
- NIH [DK091183, CA17390, DK063491]
Recent studies suggest a hierarchical model in which lineage-determining factors act in a collaborative manner to select and prime cell-specific enhancers, thereby enabling signal-dependent transcription factors to bind and function in a cell-type-specific manner. Consistent with this model, TLR4 signaling primarily regulates macrophage gene expression through a pre-existing enhancer landscape. However, TLR4 signaling also induces priming of 3,000 enhancer-like regions de novo, enabling visualization of intermediates in enhancer selection and activation. Unexpectedly, we find that enhancer transcription precedes local mono- and dimethylation of histone H3 lysine 4 (H3K4me1/2). H3K4 methylation at de novo enhancers is primarily dependent on the histone methyltransferases MII1, MII2/4, and MII3 and is significantly reduced by inhibition of RNA polymerase II elongation. Collectively, these findings suggest an essential role of enhancer transcription in H3K4me1/2 deposition at de novo enhancers that is independent of potential functions of the resulting eRNA transcripts.
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