GCN5 and E2F1 stimulate nucleotide excision repair by promoting H3K9 acetylation at sites of damage.

ABSTRACT: Chromatin structure is known to be a barrier to DNA repair and a large number of studies have now identified various factors that modify histones and remodel nucleosomes to facilitate repair. In response to ultraviolet (UV) radiation several histones are acetylated and this enhances the repair of DNA photoproducts by the nucleotide excision repair (NER) pathway. However, the molecular mechanism by which UV radiation induces histone acetylation to allow for efficient NER is not completely understood. We recently discovered that the E2F1 transcription factor accumulates at sites of UV-induced DNA damage and directly stimulates NER through a non-transcriptional mechanism. Here we demonstrate that E2F1 associates with the GCN5 acetyltransferase in response to UV radiation and recruits GCN5 to

SUBMITTER: Guo R 

PROVIDER: S-EPMC3045616 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature