Zahradka K, Zahradka D, Petranović M
Department of Molecular Genetics, Ruder Bosković Institute, Zagreb, Croatia.
Res Microbiol. 2001 Dec;152(10):873-81. doi: 10.1016/s0923-2508(01)01270-0.
Earlier studies have revealed a radiation-induced process leading to the loss of lambda prophage recombinogenicity. The process takes place in UV-irradiated Escherichia coli cells, and renders the prophage incapable of site-specific recombination with the host chromosome, and of general recombination with an infecting homologous phage. It was found that the inhibition of prophage recombinogenicity depends on functional RecBCD enzyme of E. coli. In this work, the role of ruvABC and recG genes in the inhibitory process was assessed. The products of these genes are known to act at the last step of homologous recombination and recombinational DNA repair by catalyzing the resolution of recombination intermediates (the Holliday junctions). Irradiated prophage retained its ability to recombine in ruvA, ruvB, ruvC, and recG mutants. These results suggest that in addition to RecBCD enzyme, RuvABC and RecG proteins are also involved in the inhibition of prophage recombinogenicity. We infer that RuvABC and RecG act in this process before RecBCD, probably by processing the Holliday junctions formed upon replication arrest, and thereby providing double-stranded DNA breaks as substrate for RecBCD-mediated recombinational repair of UV-damaged bacterial chromosome.
早期研究揭示了一种辐射诱导的过程,该过程导致λ原噬菌体重组活性丧失。此过程发生在紫外线照射的大肠杆菌细胞中,使原噬菌体无法与宿主染色体进行位点特异性重组,也无法与感染的同源噬菌体进行一般重组。研究发现,原噬菌体重组活性的抑制取决于大肠杆菌的功能性RecBCD酶。在这项工作中,评估了ruvABC和recG基因在抑制过程中的作用。已知这些基因的产物通过催化重组中间体(霍利迪连接体)的解离,在同源重组和重组DNA修复的最后一步发挥作用。受辐射的原噬菌体在ruvA、ruvB、ruvC和recG突变体中仍保留其重组能力。这些结果表明,除了RecBCD酶外,RuvABC和RecG蛋白也参与了原噬菌体重组活性的抑制。我们推断,RuvABC和RecG在这个过程中先于RecBCD起作用,可能是通过处理复制停滞时形成的霍利迪连接体,从而提供双链DNA断裂作为RecBCD介导的紫外线损伤细菌染色体重组修复的底物。