Pardo B, Gómez-González B, Aguilera A
Centro Andaluz de Biología Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC, Sevilla, Spain.
Cell Mol Life Sci. 2009 Mar;66(6):1039-56. doi: 10.1007/s00018-009-8740-3.
DNA double-strand breaks (DSBs) arise in cells from endogenous and exogenous attacks on the DNA backbone, but also as a direct consequence of replication failures. Proper repair of all these DSBs is essential for genome stability. Repair of broken chromosomes is a challenge for dividing cells that need to distribute equal genetic information to daughter cells. Consequently, eukaryotic organisms have evolved multi-potent and efficient mechanisms to repair DSBs that are primarily divided into two types of pathways: nonhomologous end joining (NHEJ) and homologous recombination (HR). Here we briefly describe how eukaryotic cells sense DSBs and trigger cell cycle arrest to allow repair, and we review the mechanisms of both NHEJ and HR pathways and the choice between them. (Part of a Multi-author Review).
DNA双链断裂(DSB)在细胞中由对DNA主链的内源性和外源性攻击产生,但也是复制失败的直接后果。正确修复所有这些DSB对于基因组稳定性至关重要。修复断裂的染色体对于需要将相等遗传信息分配给子细胞的分裂细胞来说是一项挑战。因此,真核生物进化出了多能且高效的机制来修复DSB,这些机制主要分为两种途径:非同源末端连接(NHEJ)和同源重组(HR)。在这里,我们简要描述真核细胞如何感知DSB并触发细胞周期停滞以进行修复,并且我们回顾NHEJ和HR途径的机制以及它们之间的选择。(多作者综述的一部分)