XRCC3 promotes homology-directed repair of DNA damage in mammalian cells
XRCC3 promotes homology-directed repair of DNA damage in mammalian cells
复制标题
DOI：
10.1101/gad.13.20.2633
复制
发表时间：
1999-10-15
影响因子：
10.5
通讯作者：
Jasin, M
中科院分区：
文献类型：
--
作者：
Pierce, AJ;Johnson, RD;Jasin, M
DNA损伤的同源性定向修复最近已成为维持哺乳动物细胞基因组完整性的主要机制。预计高度保守的链转移酶Rad51对这一过程至关重要。XRCC3具有有限的序列相似性Rad51和interactionwith it.Using一种新的基于荧光的测定，我们在这里证明，无错误的同源性指导修复DNA双链断裂减少25倍，在XRCC3缺陷仓鼠细胞系，可以恢复到野生型水平，通过XRCC3的表达。这些结果表明，XRCC3介导的同源重组可以逆转DNA损伤，否则将是致突变或致命的。
Homology-directed repair of DNA damage has recently emerged as a major mechanism for the maintenance of genomic integrity in mammalian cells. The highly conserved strand transferase, Rad51, is expected to be critical for this process. XRCC3 possesses a limited sequence similarity to Rad51 and interacts with it. Using a novel fluorescence-based assay, we demonstrate here that error-free homology-directed repair of DNA double-strand breaks is decreased 25-fold in an XRCC3-deficient hamster cell line and can be restored to wild-type levels through XRCC3 expression. These results establish that XRCC3-mediated homologous recombination can reverse DNA damage that would otherwise be mutagenic or lethal.