Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 13, Issue 10, Pages 13554-13568Publisher
MDPI
DOI: 10.3390/ijms131013554
Keywords
DNA repair; chromatin; histone acetylation; GCN5; p300
Funding
- National Institutes of Health through MD Anderson's Cancer Center [CA016672]
- National Cancer Institute [R01CA79648]
- National Institute of Environmental Health Sciences Center [ES007784]
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Many of the biochemical details of nucleotide excision repair (NER) have been established using purified proteins and DNA substrates. In cells however, DNA is tightly packaged around histones and other chromatin-associated proteins, which can be an obstacle to efficient repair. Several cooperating mechanisms enhance the efficiency of NER by altering chromatin structure. Interestingly, many of the players involved in modifying chromatin at sites of DNA damage were originally identified as regulators of transcription. These include ATP-dependent chromatin remodelers, histone modifying enzymes and several transcription factors. The p53 and E2F1 transcription factors are well known for their abilities to regulate gene expression in response to DNA damage. This review will highlight the underappreciated, transcription-independent functions of p53 and E2F1 in modifying chromatin structure in response to DNA damage to promote global NER.
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