Error-free recombinational repair predominates over mutagenic translesion replication in E-coli
Error-free recombinational repair predominates over mutagenic translesion replication in E-coli
复制标题
DOI：
10.1016/s1097-2765(02)00679-2
复制
发表时间：
2002-10-01
期刊：
影响因子：
16
通讯作者：
Livneh, Z
中科院分区：
文献类型：
--
作者：
Berdichevsky, A;Izhar, L;Livneh, Z
耐受机制在细胞科普DNA损伤的能力中是重要的。在大肠在大肠杆菌中，两种主要的损伤耐受机制是重组修复（RR）和跨损伤复制（TLR）。在这里，我们表明，FIR有效地修复缺口对面的DNA损伤。当两种机制都起作用时，FIR比TLR占主导地位，负责86%的修复事件。FIR的这种优势是由SOS条件下存在的高浓度RecA决定的，这导致TLR的差异抑制。TLR的进一步抑制由FIR的RecA催化的链交换反应引起。这种DNA损伤耐受性的分子层次确保了非致突变FIR优于致突变TLR，从而有助于遗传稳定性。
Tolerance mechanisms are important in the ability of cells to cope with DNA damage. In E. coli, the two main damage tolerance mechanisms are recombinational repair (RR) and translesion replication (TLR). Here we show that FIR effectively repairs gaps opposite DNA lesions. When both mechanisms are functional, FIR predominates over TLR, being responsible for 86% of the repair events. This predominance of FIR is determined by the high concentration of RecA present under SOS conditions, which causes a differential inhibition of TLR. Further inhibition of TLR is caused by the RecA-catalyzed strand exchange reaction of FIR. This molecular hierarchy in the tolerance of DNA lesions ensures that the nonmutagenic FIR predominates over the mutagenic TLR, thereby contributing to genetic stability.