Mandal T N, Mahdi A A, Sharples G J, Lloyd R G
Department of Genetics, University of Nottingham, Queens Medical Centre, United Kingdom.
J Bacteriol. 1993 Jul;175(14):4325-34. doi: 10.1128/jb.175.14.4325-4334.1993.
The ruvA, ruvB, and ruvC genes of Escherichia coli provide activities that catalyze branch migration and resolution of Holliday junction intermediates in recombination. Mutation of any one of these genes interferes with recombination and reduces the ability of the cell to repair damage to DNA. A suppressor of ruv mutations was identified on the basis of its ability to restore resistance to mitomycin and UV light and to allow normal levels of recombination in a recBC sbcBC strain carrying a Tn10 insertion in ruvA. The mutation responsible was located at 12.5 min on the genetic map and defines a new locus which has been designated rus. The rus suppressor works just as well in recBC sbcA and rec+ sbc+ backgrounds and is not allele specific. Mutations in ruvB and ruvC are suppressed to an intermediate level, except when ruvA is also inactive, in which case suppression is complete. In all cases, suppression depends on RecG protein, a DNA-dependent ATPase that catalyzes branch migration of Holliday junctions. The rus mutation activates an additional factor that probably works with RecG to process Holliday junction intermediates independently of the RuvAB and RuvC proteins. The possibility that this additional factor is a junction-specific resolvase is discussed.
大肠杆菌的ruvA、ruvB和ruvC基因所提供的活性可催化重组过程中霍利迪连接中间体的分支迁移和拆分。这些基因中任何一个发生突变都会干扰重组，并降低细胞修复DNA损伤的能力。基于其恢复对丝裂霉素和紫外线的抗性以及使携带ruvA中Tn10插入片段的recBC sbcBC菌株进行正常水平重组的能力，鉴定出了ruv突变的一个抑制子。导致该抑制作用的突变位于遗传图谱的12.5分钟处，定义了一个新的基因座，已将其命名为rus。rus抑制子在recBC sbcA和rec+ sbc+背景中同样有效，且不具有等位基因特异性。ruvB和ruvC中的突变被抑制到中等水平，除非ruvA也无活性，在这种情况下抑制作用是完全的。在所有情况下，抑制作用都依赖于RecG蛋白，这是一种DNA依赖性ATP酶，可催化霍利迪连接的分支迁移。rus突变激活了一个额外的因子，该因子可能与RecG协同作用，独立于RuvAB和RuvC蛋白来处理霍利迪连接中间体。本文讨论了这个额外因子是一种连接特异性拆分酶的可能性。
