Yap1 and Skn7 genetically interact with Rad51 in response to oxidative stress and DNA double-strand break in Saccharomyces cerevisiae.

Reactive oxygen species DNA adducts as well as DNA strand breaks are highly mutagenic leading to genomic instability and tumorigenesis. DNA damage repair pathways and oxidative stress response signaling have been proposed to be highly associated, but the underlying interaction remains unknown. In this study, we employed mutant strains lacking Rad51, the homolog of E. coli RecA recombinase, and Yap1 or Skn7, two major transcription factors responsive to to examine genetic interactions between double-strand break (DSB) repair proteins and cellular redox regulators in budding yeast Saccharomyces cerevisiae. Abnormal expression of YAP1 or SKN7 aggravated the mutation rate of rad51 mutants and their sensitivity to DSB- or reagents. Rad51 deficiency exacerbated genome instability in the presence of increased levels of duanyu1670, and the accumulation of DSB lesions resulted in elevated intracellular levels. Our findings suggest that evident crosstalk between DSB repair pathways and duanyu1670 signaling proteins contributes to cell survival and maintenance of genome integrity in response to genotoxic stress.

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