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

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


  • Gong F
  • Fahy D
  • Smerdon MJ


Nature structural & molecular biology

Publication Data

October 5, 2006

Associated Grants

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

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