Homologous recombination is essential for the maintenance of genome integrity but must be strictly controlled to avoid dangerous outcomes that produce the opposite effect, genomic instability. During unperturbed chromosome replication, recombination is globally inhibited at ongoing DNA replication forks, which helps to prevent deleterious genomic rearrangements. This inhibition is carried out by Srs2, a helicase that binds to SUMOylated PCNA and has an anti-recombinogenic function at replication forks. However, at damaged stalled forks, Srs2 is counteracted and DNA lesion bypass can be achieved by recombination-mediated template switching. In budding yeast, template switching is dependent on Rad5. In the absence of this protein, replication forks stall in the presence of DNA lesions and cells die. Recently, we showed that in cells lacking Rad5 that are exposed to DNA damage or replicative stress, elimination of the conserved Mgs1/WRNIP1 ATPase allows an alternative mode of DNA damage bypass that is driven by recombination and facilitates completion of chromosome replication and cell viability. We have proposed that Mgs1 is important to prevent a potentially harmful salvage pathway of recombination at damaged stalled forks. In this review, we summarize our current understanding of how unwanted recombination is prevented at damaged stalled replication forks.

同源重组对于维持基因组完整性至关重要，但必须严格控制，以避免产生相反作用的危险结果，即基因组不稳定。在染色体复制不受干扰的过程中，重组在正在进行的DNA复制叉处被全面抑制，这有助于防止有害的基因组重排。这种抑制作用由Srs2进行，Srs2是一种与SUMO酰化PCNA结合的解旋酶，在复制叉处具有抗重组的功能。然而，在损坏的失速叉上，Srs2被抵消，DNA损伤旁路可以通过重组介导的模板转换来实现。在发芽酵母中，模板转换取决于Rad5。在缺乏这种蛋白质的情况下，复制叉会在存在DNA损伤的情况下停滞并且细胞死亡。最近，我们发现，在缺少Rad5的细胞中暴露于DNA损伤或复制压力下，消除保守的Mgs1 / WRNIP1 ATPase可以通过重组驱动DNA损伤旁路的另一种模式，并有助于完成染色体复制和细胞活力。我们已经提出，Mgs1对于防止损坏的失速叉中重组的潜在有害挽救途径很重要。在这篇综述中，我们总结了当前对如何防止损坏的停滞的复制叉处不必要的重组的理解。我们已经提出，Mgs1对于防止损坏的失速叉中重组的潜在有害挽救途径很重要。在这篇综述中，我们总结了当前对如何防止损坏的停滞的复制叉处不必要的重组的理解。我们已经提出，Mgs1对于防止损坏的失速叉中重组的潜在有害挽救途径很重要。在这篇综述中，我们总结了我们目前的理解，即如何在损坏的停滞的复制叉处防止不必要的重组。