H3K4me3 Interactions with TAF3 Regulate Preinitiation Complex Assembly and Selective Gene Activation
Open accessAbstract
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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Target genes were reported to be activated by p53 with varying kinetics through stimulus- and promoter-specific recruitment of transcription initiation components and polymerase II.
“Target genes were reported to be activated by p53 with varying kinetics through stimulus- and promoter-specific recruitment of transcription initiation components and polymerase II.60, 61, 62, 63”
From Census and evaluation of p53 target genes (2017) · cites this paper as [62]
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References 61 · Cited by 473
- Authors
- Lauberth, S. M., Nakayama, T., Wu, X., Ferris, A. L., Tang, Z., Hughes, S. H., & Roeder, R. G.
- Affiliations
- Rockefeller University (US)
- Frederick National Laboratory for Cancer Research (US)
- National Cancer Institute (US)
- Corresponding author
- Roeder, Robert G.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-02
- Volume
- 152
- Issue
- 5
- Pages
- 1021-1036
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3588593
- OpenAlex
- W2120100277
- Cited by
- 473
- References
- 61
- Citations by year
- 2026: 30 · 2025: 42 · 2024: 50 · 2023: 35 · 2022: 28 · 2021: 36 · 2020: 35 · 2019: 29 · 2018: 29 · 2017: 33 · 2016: 33 · 2015: 33 · 2014: 37 · 2013: 22
- FWCI
- 18.98
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- National Cancer Institute (CA129325, CA 09673, R01CA129325, T32CA009673)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK071900, DK 071900)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- H3K4me3, TAF3, TFIID, preinitiation complex assembly, p53-dependent transcription, histone modifications, TATA box, genotoxic stress response, p53 target genes, chromatin regulation, transcriptional activation
- MeSH terms
- Histones, Humans, Lysine, Methylation, Transcriptional Activation, Tumor Suppressor Protein p53, TATA Box, Transcription Factor TFIID, TATA-Binding Protein Associated Factors, Histone Code, Cell Line, Tumor, p300-CBP Transcription Factors, Transcription Initiation, Genetic
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