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Resolving RAD51C function in late stages of homologous recombination

机译：在同源重组的后期解决RAD51C功能

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DNA double strand breaks are efficiently repaired by homologous recombination. One of the last steps of this process is resolution of Holliday junctions that are formed at the sites of genetic exchange between homologous DNA. Although various resolvases with Holliday junctions processing activity have been identified in bacteriophages, bacteria and archaebacteria, eukaryotic resolvases have been elusive. Recent biochemical evidence has revealed that RAD51C and XRCC3, members of the RAD51-like protein family, are involved in Holliday junction resolution in mammalian cells. However, purified recombinant RAD51C and XRCC3 proteins have not shown any Holliday junction resolution activity. In addition, these proteins did not reveal the presence of a nuclease domain, which raises doubts about their ability to function as a resolvase. Furthermore, oocytes from infertile Rad51C mutant mice exhibit precocious separation of sister chromatids at metaphase II, a phenotype that reflects a defect in sister chromatid cohesion, not a lack of Holliday junction resolution. Here we discuss a model to explain how a Holliday junction resolution defect can lead to sister chromatid separation in mouse oocytes. We also describe other recent in vitro and in vivo evidence supporting a late role for RAD51C in homologous recombination in mammalian cells, which is likely to be resolution of the Holliday junction.
机译：DNA双链断裂可通过同源重组得到有效修复。该过程的最后步骤之一是解析在同源DNA之间的遗传交换位点形成的霍利迪连接。尽管已经在噬菌体，细菌和古细菌中鉴定出了具有霍利迪接头加工活性的各种分辨物，但真核分辨物却难以捉摸。最近的生化证据表明，RAD51-like蛋白家族的成员RAD51C和XRCC3参与哺乳动物细胞中的霍利迪连接解析。但是，纯化的重组RAD51C和XRCC3蛋白没有显示出任何霍利迪连接分辨活性。另外，这些蛋白质没有揭示核酸酶结构域的存在，这使人们怀疑它们是否具有作为分辨酶的功能。此外，来自不育的Rad51C突变小鼠的卵母细胞在中期II处表现出姐妹染色单体的早熟分离，这种表型反映了姐妹染色单体内聚力的缺陷，而不是缺乏霍利迪接头的分辨率。在这里，我们讨论一个模型来解释霍利迪结分辨率缺陷如何导致小鼠卵母细胞中姐妹染色单体分离。我们还描述了其他最新的体外和体内证据，这些证据支持RAD51C在哺乳动物细胞中同源重组中的后期作用，这很可能是霍利迪交界处的分辨率。

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