During DNA replication, stalling can occur when the replicative DNA polymerases encounter lesions or hard-to replicate regions. Under these circumstances, the processivity factor PCNA gets ubiquitylated at lysine 164, inducing the DNA damage tolerance (DDT) mechanisms that can bypass lesions encountered during DNA replication. PCNA can also be SUMOylated at the same residue or at lysine 127. Surprisingly, pol30-K164R mutants display a higher degree of sensitivity to DNA-damaging agents than pol30-KK127,164RR strains, unable to modify any of the lysines. Here, we show that in addition to translesion synthesis and strand-transfer DDT mechanisms, an alternative repair mechanism (“salvage recombination”) that copies information from the sister chromatid is repressed by the recruitment of Srs2 to SUMOylated PCNA. Overexpression of Elg1, the PCNA unloader, or of the recombination protein Rad52 allows its activation. We dissect the genetic requirements for this pathway, as well as the interactions between Srs2 and Elg1.

中文翻译：

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Srs2和Elg1对PCNA的访问控制了酿酒酵母中其他修复途径之间的选择。

在DNA复制期间，当复制性DNA聚合酶遇到损伤或难以复制的区域时，可能发生停转。在这些情况下，生产力因子PCNA在赖氨酸164处被泛素化，从而诱导了DNA损伤耐受（DDT）机制，可以绕过DNA复制过程中遇到的损伤。PCNA也可以在相同的残基或赖氨酸127 SUMO化令人惊讶地，pol30-K164R突变体显示更高的灵敏度对DNA损伤剂比pol30-KK127,164RR菌株，无法修饰任何赖氨酸。在这里，我们表明，除了跨病变合成和链转移DDT机制外，Srs2募集到SUMOylated PCNA还抑制了从姐妹染色单体复制信息的替代修复机制（“挽救重组”）。Elg1，PCNA卸载子或重组蛋白Rad52的过表达允许其激活。我们剖析了这种途径的遗传要求，以及Srs2和Elg1之间的相互作用。