Whitby M C, Bolt E L, Chan S N, Lloyd R G
Department of Genetics, University of Nottingham, Queens Medical Centre, UK.
J Mol Biol. 1996 Dec 20;264(5):878-90. doi: 10.1006/jmbi.1996.0684.
The RuvAB and RuvC enzymes of Escherichia coli define a molecular pathway for the resolution of Holliday intermediates in recombination and DNA repair. They bind specifically to Holliday junctions, and catalyse their branch migration and cleavage, respectively. In a RuvA(B)-junction complex, the Holliday structure is held in an open (square planar) configuration on the concave surface of a 4-fold symmetrical tetramer of RuvA, whereas in a RuvC-junction complex it is folded in an alternative arrangement as part of the cleavage reaction. Genetic studies have shown that the activity of RuvC in vivo depends on RuvAB, which suggests that the two enzymes act in concert, with junction cleavage by RuvC following from branch migration by RuvAB. We have investigated how RuvC can take over a junction from RuvAB to cleave the DNA. We show that RuvA inhibits junction cleavage by RuvC, probably by sandwiching the junction between two tetramers. The extent of inhibition depends on the reaction kinetics of RuvA binding relative to RuvC binding and cleavage. The presence of RuvB and the concentration of Mg2+ both have a significant effect on cleavage in the presence of RuvA. However, a novel protein-DNA complex can be formed when junction DNA is incubated with both RuvA and RuvC. Its mobility is consistent with a RuvC dimer binding to a junction held in an open configuration on the surface of a RuvA tetramer. We suggest that this arrangement provides RuvC with the means to scan the junction during the RuvAB-mediated branch migration reaction for DNA sequences that it can cleave. We further suggest that recognition of the target may provide a trigger for dissociating RuvA, allowing the junction to be folded and cleaved by RuvC.
大肠杆菌的RuvAB和RuvC酶确定了一条在重组和DNA修复过程中解析霍利迪中间体的分子途径。它们特异性结合霍利迪连接点,并分别催化其分支迁移和切割。在RuvA(B)-连接点复合物中,霍利迪结构以开放(方形平面)构象保持在RuvA四聚体凹面的4重对称表面上,而在RuvC-连接点复合物中,它作为切割反应的一部分以另一种排列方式折叠。遗传学研究表明,RuvC在体内的活性依赖于RuvAB,这表明这两种酶协同作用,RuvC的连接点切割发生在RuvAB的分支迁移之后。我们研究了RuvC如何从RuvAB接管连接点以切割DNA。我们发现RuvA抑制RuvC的连接点切割,可能是通过将连接点夹在两个四聚体之间。抑制程度取决于RuvA结合相对于RuvC结合和切割的反应动力学。RuvB的存在和Mg2+的浓度在有RuvA存在时对切割都有显著影响。然而,当连接点DNA与RuvA和RuvC一起孵育时,可以形成一种新的蛋白质-DNA复合物。其迁移率与RuvC二聚体结合到RuvA四聚体表面上以开放构象保持的连接点一致。我们认为这种排列为RuvC提供了一种在RuvAB介导的分支迁移反应过程中扫描连接点以寻找其可切割的DNA序列的方式。我们进一步认为对靶标的识别可能提供了一个解离RuvA的触发因素,使连接点能够被RuvC折叠并切割。