Gong Feng, Fahy Deirdre, Smerdon Michael J
Biochemistry and Biophysics, School of Molecular Biosciences, Washington State University, Pullman, Washington 99164-4660, USA.
Nat Struct Mol Biol. 2006 Oct;13(10):902-7. doi: 10.1038/nsmb1152. Epub 2006 Oct 1.
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.
染色质重排发生在核苷酸切除修复(NER)过程中。我们在此表明,酿酒酵母中SWI/SNF染色质重塑复合物的两个亚基Snf6和Snf5与NER损伤识别异源二聚体Rad4-Rad23共同纯化。SWI/SNF与Rad4-Rad23之间的这种相互作用受紫外线照射刺激。我们证明,在缺乏功能性SWI/SNF的酵母细胞中,转录沉默、核小体负载的HML位点的NER减少。此外,使用限制性内切酶可及性测定法,我们在沉默的HML位点观察到紫外线诱导的核小体重排。值得注意的是,当SWI/SNF失活时,这种重排明显减弱。这些结果表明,SWI/SNF染色质重塑复合物被损伤识别蛋白招募到DNA损伤处,以增加染色质中NER的DNA可及性。