Matteo Di Terlizzi, Giordano Liberi, Achille Pellicioli
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引用次数: 0
摘要
所有细胞通常都会受到 DNA 双链断裂(DSB)的影响,必须对其进行适当的修复,以避免基因组的不稳定性。断裂诱导复制(BIR)是一种同源重组子途径,可修复导致突变、染色体易位和杂合性丧失的 DSB。在芽殖酵母中,Srs2 DNA螺旋酶/反转录酶既起抗重组作用,也起促重组作用。有趣的是,Srs2 的活动是支持 BIR 完成所必需的。在这里,我们采用了染色体间 BIR 试验来描述 Srs2 的 Cdk1 依赖性磷酸化、ATPase 和螺旋酶活性。我们的研究结果进一步拓展了我们对 Srs2 在 DSB 重组修复中所扮演的多面角色的理解。
Separation of function mutants underline multiple roles of the Srs2 helicase/translocase in break-induced replication in Saccharomyces cerevisiae.
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.