| Literature DB >> 18026119 |
Su Wu1, Yujiang Shi, Peter Mulligan, Frédérique Gay, Joseph Landry, Huifei Liu, Ju Lu, Hank H Qi, Weijia Wang, Jac A Nickoloff, Carl Wu, Yang Shi.
Abstract
DNA damage repair is crucial for the maintenance of genome integrity and cancer suppression. We found that loss of the mouse transcription factor YY1 resulted in polyploidy and chromatid aberrations, which are signatures of defects in homologous recombination. Further biochemical analyses identified a YY1 complex comprising components of the evolutionarily conserved INO80 chromatin-remodeling complex. Notably, RNA interference-mediated knockdown of YY1 and INO80 increased cellular sensitivity toward DNA-damaging agents. Functional assays revealed that both YY1 and INO80 are essential in homologous recombination-based DNA repair (HRR), which was further supported by the finding that YY1 preferentially bound a recombination-intermediate structure in vitro. Collectively, these observations reveal a link between YY1 and INO80 and roles for both in HRR, providing new insight into mechanisms that control the cellular response to genotoxic stress.Entities:
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Year: 2007 PMID： 18026119 PMCID： PMC2754171 DOI： 10.1038/nsmb1332
Source DB: PubMed Journal: Nat Struct Mol Biol ISSN： 1545-9985 Impact factor: 15.369