Seigneur M, Bidnenko V, Ehrlich S D, Michel B
Génétique Microbienne, Institute National de la Recherche Agronomique, Jouy en Josas, France.
Cell. 1998 Oct 30;95(3):419-30. doi: 10.1016/s0092-8674(00)81772-9.
Replication arrest leads to the occurrence of DNA double-stranded breaks (DSB). We studied the mechanism of DSB formation by direct measure of the amount of in vivo linear DNA in Escherichia coli cells that lack the RecBCD recombination complex and by genetic means. The RuvABC proteins, which catalyze migration and cleavage of Holliday junctions, are responsible for the occurrence of DSBs at arrested replication forks. In cells proficient for RecBC, RuvAB is uncoupled from RuvC and DSBs may be prevented. This may be explained if a Holliday junction forms upon replication fork arrest, by annealing of the two nascent strands. RecBCD may act on the double-stranded tail prior to the cleavage of the RuvAB-bound junction by RuvC to rescue the blocked replication fork without breakage.
复制停滞会导致DNA双链断裂（DSB）的发生。我们通过直接测量缺乏RecBCD重组复合物的大肠杆菌细胞中体内线性DNA的量，并采用遗传学方法，研究了DSB形成的机制。催化霍利迪连接体迁移和切割的RuvABC蛋白，是导致停滞复制叉处出现DSB的原因。在RecBC功能正常的细胞中，RuvAB与RuvC解偶联，从而可能防止DSB的发生。如果在复制叉停滞时，两条新生链退火形成霍利迪连接体，或许可以解释这一现象。在RuvC切割与RuvAB结合的连接体之前，RecBCD可能作用于双链尾巴，以挽救受阻的复制叉而不发生断裂。
