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Rad4-Rad23 interaction with SWI/SNF links ATP-dependent chromatin remodeling with nucleotide excision repair.

http://www.ncbi.nlm.nih.gov/pubmed/17013386

Chromatin rearrangement occurs during nucleotide excision repair (NER). Here we show that Snf6 and Snf5, two subunits of the SWI/SNF chromatin-remodeling complex in Saccharomyces cerevisiae, copurify with the NER damage-recognition heterodimer Rad4-Rad23. This interaction between SWI/SNF and Rad4-Rad23 is stimulated by UV irradiation. We demonstrate that NER in the transcriptionally silent, nucleosome-loaded HML locus is reduced in yeast cells lacking functional SWI/SNF. In addition, using a restriction enzyme accessibility assay, we observed UV-induced nucleosome rearrangement at the silent HML locus. Notably, this rearrangement is markedly attenuated when SWI/SNF is inactivated. These results indicate that the SWI/SNF chromatin-remodeling complex is recruited to DNA lesions by damage-recognition proteins to increase DNA accessibility for NER in chromatin.

Pubmed ID: 17013386 RIS Download

Mesh terms: Adenosine Triphosphate | Cells, Cultured | Chromatin | Chromatin Assembly and Disassembly | Chromosomal Proteins, Non-Histone | DNA Repair | DNA-Binding Proteins | Models, Biological | Models, Molecular | Saccharomyces cerevisiae Proteins | Transcription Factors

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Associated grants

  • Agency: NIEHS NIH HHS, Id: ES02614
  • Agency: NIEHS NIH HHS, Id: ES04106

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