Deletion of IRC19 Causes Defects in DNA Double-Strand Break Repair Pathways in Saccharomyces cerevisiae

초록

DNA double-strand break (DSB) repair is a fundamental cellular process crucial for maintaining genome stability, with homologous recombination and non-homologous end joining as the primary mechanisms, and various alternative pathways such as single-strand annealing (SSA) and microhomology-mediated end joining also playing significant roles under specific conditions. IRC genes were previously identified as part of a group of genes associated with increased levels of Rad52 foci in Saccharomyces cerevisiae. In this study, we investigated the effects of IRC gene mutations on DSB repair, focusing on uncharacterized IRC10, 19, 21, 22, 23, and 24. Gene conversion (GC) assay revealed that irc10 Delta, 22 Delta, 23 Delta, and 24 Delta mutants displayed modest increases in GC frequencies, while irc19 Delta and irc21 Delta mutants exhibited significant reductions. Further investigation revealed that deletion mutations in URA3 were not generated in irc19 Delta mutant cells following HO-induced DSBs. Additionally, irc19 Delta significantly reduced frequency of SSA, and a synergistic interaction between irc19 Delta and rad52 Delta was observed in DSB repair via SSA. Assays to determine the choice of DSB repair pathways indicated that Irc19 is necessary for generating both GC and deletion products. Overall, these results suggest a potential role of Irc19 in DSB repair pathways, particularly in end resection process.

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