Separation of function mutants underline multiple roles of the Srs2 helicase/translocase in break-induced replication in Saccharomyces cerevisiae.

Abstract

All cells are commonly exposed to DNA double-strand breaks (DSBs), which must be properly repaired to avoid genomic instability. Break-Induced Replication (BIR) is a Homologous Recombination subpathway, which repairs DSBs resulting in mutagenesis, chromosome translocations and loss of heterozygosity. In budding yeast, the Srs2 DNA helicase/translocase plays both anti- and pro-recombination roles. Interestingly, Srs2 activities are required to support BIR completion. Here, we employ a interchromosomal BIR assay in S. cerevisiae to characterize Cdk1-dependent phosphorylation, ATPase and helicase activities of Srs2. Our results further expand our understanding of the multifaced role played by Srs2 in DSB recombination repair.