Kang Josephine, Blaser Martin J
Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.
J Bacteriol. 2008 Jun;190(12):4218-24. doi: 10.1128/JB.01848-07. Epub 2008 Mar 28.
Orthologs of RecG and RuvABC are highly conserved among prokaryotes; in Escherichia coli, they participate in independent pathways that branch migrate Holliday junctions during recombinational DNA repair. RecG also has been shown to directly convert stalled replication forks into Holliday junctions. The bacterium Helicobacter pylori, with remarkably high levels of recombination, possesses RecG and RuvABC homologs, but in contrast to E. coli, H. pylori RecG limits recombinational repair. We now show that the RuvABC pathway plays the prominent, if not exclusive, repair role. By introducing an E. coli resolvase (RusA) into H. pylori, the repair and recombination phenotypes of the ruvB mutant but not the recG mutant were improved. Our results indicate that RecG and RuvB compete for Holliday junction structures in recombinational repair, but since a classic RecG resolvase is absent from H. pylori, deployment of the RecG pathway is lethal. We propose that evolutionary loss of the H. pylori RecG resolvase provides an "antirepair" pathway allowing for selection of varied strains. Such competition between repair and antirepair provides a novel mechanism to maximize fitness at a bacterial population level.
RecG和RuvABC的直系同源基因在原核生物中高度保守；在大肠杆菌中，它们参与在重组DNA修复过程中对霍利迪连接体进行分支迁移的独立途径。RecG也已被证明能直接将停滞的复制叉转化为霍利迪连接体。幽门螺杆菌这种细菌具有非常高的重组水平，拥有RecG和RuvABC的同源物，但与大肠杆菌不同的是，幽门螺杆菌的RecG会限制重组修复。我们现在表明，RuvABC途径发挥着突出的（如果不是唯一的）修复作用。通过将一种大肠杆菌解离酶（RusA）引入幽门螺杆菌，ruvB突变体而非recG突变体的修复和重组表型得到了改善。我们的结果表明，在重组修复中，RecG和RuvB竞争霍利迪连接体结构，但由于幽门螺杆菌中不存在经典的RecG解离酶，RecG途径的发挥是致命的。我们提出，幽门螺杆菌RecG解离酶的进化缺失提供了一种“抗修复”途径，从而允许选择不同的菌株。这种修复与抗修复之间的竞争提供了一种在细菌群体水平上使适应性最大化的新机制。
