Analysis of a new mechanism on homology-dependent repair

为了阐明NBS1与RAD51物理相互作用的生物学意义，我们试图建立一个不能与RAD51结合的NBS1突变体。在这个过程中，我们发现NBS1通过MRE11与RAD51相互作用。不与RAD51相互作用的MRE11突变体具有完全的同源依赖修复DNA双链断裂（DSBs）活性。表达MRE11突变体的细胞对电离辐射不敏感。这些结果表明，NBS1和RAD51之间的相互作用在DSB修复中没有重要作用，但在其他机制中起作用。

In order to clarify the biological significance of the physical interaction between NBS1 and RAD51, we tried to establish a NBS1 mutant that was not able to bind to RAD51. In this process, we found that NBS1 interacted with RAD51 through MRE11. The MRE11 mutant that could not interact with RAD51 had full activity of homology-dependent repair of DNA double-strand breaks(DSBs). Cells expressing the MRE11 mutant did not show sensitivity to ionizing radiation. These results indicate that the interaction between NBS1 and RAD51 does not have an important role in DSB repair but has a role in other mechanisms.