Abstract:Defects in repair of DNA double-strand breaks (DSBs) can lead to genome instability, tumorigenesis or cell death. Eukaryotic cells employ two major pathways, homologous recombination (HR) and non-homologous end joining (NHEJ), to repair DSBs. Recent studies have revealed that several ATP-dependent chromatin remodeling complexes, including RSC, INO80, Fun30, SWI/SNF and SWR1, play direct roles in DSB repair. These remodeling factors exert critical functions at multiple key steps in DSB repair, such as DNA damage checkpoint activation, end processing or H2AZ-H2B/H2A-H2B exchange. In this review, we summarized recent progresses on this topic with an emphasis on the roles and mechanisms of these chromatin remodeling factors in Saccharomyces cerevisiae.