期刊
MOLECULAR CELL
卷 51, 期 2, 页码 185-199出版社
CELL PRESS
DOI: 10.1016/j.molcel.2013.06.007
关键词
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资金
- NCI Cancer Center [5 P30 CA125123]
- National Institutes of Health [5 R01 HD008188, 2 P01 DK059820, 5 K01 DK084209, P30DK079638PJ4]
- Welch Foundation [Q-152]
Chromatin immunoprecipitation studies have mapped protein occupancies at many genomic loci. However, a detailed picture of the complexity of coregulators (CoRs) bound to a defined enhancer along with a transcription factor is missing. To address this, we used biotin-DNA pull-down assays coupled with mass spectrometry-immunoblotting to identify at least 17 CoRs from nuclear extracts bound to 17 beta-estradiol (E2)-liganded estrogen receptor-alpha on estrogen response elements (EREs). Unexpectedly, these complexes initially are biochemically stable and contain certain atypical corepressors. Addition of ATP dynamically converts these complexes to an activated state by phosphorylation events, primarily mediated by DNA-dependent protein kinase. Importantly, a natural ERE-containing enhancer and nucleosomal EREs recruit similar complexes. We further discovered the mechanism whereby H3K4me3 stimulates ER alpha-mediated transcription as compared with unmodified nucleosomes. H3K4me3 templates promote specific CoR dynamics in the presence of ATP and AcCoA, as manifested by CBP/p300 and SRC-3 dismissal and SAGA and TFIID stabilization/recruitment.
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