DNA polymerases sometimes stall during DNA replication at sites where DNA is damaged, or upon encounter with proteins or secondary structures of DNA. When that happens, the polymerase clamp PCNA can become modified with a single ubiquitin moiety at lysine 164, opening DNA Damage Tolerance (DDT) mechanisms that either repair or bypass the lesions. An alternative repair mechanism is the salvage recombination (SR) pathway, which copies information from the sister chromatid. SUMOylation of PCNA at the same lysine, or at lysine 127, can recruit the Srs2 helicase, which negatively controls SR. Recently, we have dissected the relationship between SR and the DDT pathways, and showed that overexpression of either the PCNA unloader Elg1, or the Rad52 homologous recombination protein, can bypass the repression by Srs2. Our results shed light on the interactions between different DNA damage repair/bypass proteins, and underscore the importance of PCNA modifications in organizing the complex task of dealing with DNA damage during replication of the genetic material.

中文翻译：

---

酵母细胞如何处理停滞的复制叉。

DNA聚合酶有时会在DNA复制过程中停滞在DNA受损的位置，或者遇到蛋白质或DNA二级结构时停滞。发生这种情况时，聚合酶钳PCNA可以被赖氨酸164处的单个泛素部分修饰，从而打开修复或绕过病变的DNA损伤耐受（DDT）机制。另一种修复机制是补救重组（SR）途径，该途径可复制姐妹染色单体的信息。PCNA在相同的赖氨酸或127赖氨酸上的SUMOylation可以募集Srs2解旋酶，对SR产生负调控。最近，我们已经剖析了SR和DDT途径之间的关系，并表明PCNA卸载子Elg1或Rad52同源重组蛋白的过表达可以绕过Srs2的抑制。