Journal
CELL
Volume 152, Issue 5, Pages 1021-1036Publisher
CELL PRESS
DOI: 10.1016/j.cell.2013.01.052
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Funding
- NRSA [CA 09673]
- NIH, Center for Cancer Research, National Cancer Institute
- NIH [CA129325, DK071900]
- Leukemia and Lymphoma Society [7132-08]
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Histone modifications regulate chromatin-dependent processes, yet the mechanisms by which they contribute to specific outcomes remain unclear. H3K4me3 is a prominent histone mark that is associated with active genes and promotes transcription through interactions with effector proteins that include initiation factor TFIID. We demonstrate that H3K4me3-TAF3 interactions direct global TFIID recruitment to active genes, some of which are p53 targets. Further analyses show that (1) H3K4me3 enhances p53-dependent transcription by stimulating preinitiation complex (PIC) formation; (2) H3K4me3, through TAF3 interactions, can act either independently or cooperatively with the TATA box to direct PIC formation and transcription; and (3) H3K4me3-TAF3/TFIID interactions regulate gene-selective functions of p53 in response to genotoxic stress. Our findings indicate a mechanism by which H3K4me3 directs PIC assembly for the rapid induction of specific p53 target genes.
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