Completion of DNA replication in Escherichia coli.
Completion of DNA replication in Escherichia coli.
复制标题
在大肠杆菌中完成 DNA 复制。
DOI：
10.1073/pnas.1415025111
复制
发表时间：
2014
影响因子：
11.1
通讯作者：
Courcelle,Justin
中科院分区：
文献类型：
--
作者：
Wendel,BrianM;Courcelle,CharmainT;Courcelle,Justin
细胞在精确的倍增点识别和完成复制区域的机制必须非常有效，沿着人类染色体沿着的每一次细胞分裂都发生数千次。然而，对这一过程的了解仍然很少。在这里，我们表明，在大肠杆菌，复制的完成涉及到一个酶系统，有效地计数对和限制细胞复制到其倍增点，允许收敛复制叉暂时继续通过倍增点之前，多余的，过度复制的区域被切开，切除，并加入。完成需要RecBCD，并涉及与修复双链断裂相关的几种蛋白质，包括ExoI，SbcDC和RecG。然而，与双链断裂修复不同，完成独立于同源重组和RecA发生。在一些细菌病毒中，完成机制专门针对灭活，以允许在裂解复制期间发生过度复制。结果表明，在许多双链断裂修复突变体的基因组不稳定性的主要原因是从一个受损的能力，完成复制，独立于DNA损伤。
The mechanism by which cells recognize and complete replicated regions at their precise doubling point must be remarkably efficient, occurring thousands of times per cell division along the chromosomes of humans. However, this process remains poorly understood. Here we show that, inEscherichia coli, the completion of replication involves an enzymatic system that effectively counts pairs and limits cellular replication to its doubling point by allowing converging replication forks to transiently continue through the doubling point before the excess, over-replicated regions are incised, resected, and joined. Completion requires RecBCD and involves several proteins associated with repairing double-strand breaks including, ExoI, SbcDC, and RecG. However, unlike double-strand break repair, completion occurs independently of homologous recombination and RecA. In some bacterial viruses, the completion mechanism is specifically targeted for inactivation to allow over-replication to occur during lytic replication. The results suggest that a primary cause of genomic instabilities in many double-strand-break-repair mutants arises from an impaired ability to complete replication, independent from DNA damage.