Chung Kuei-Min, Hsu Hsin-Hsien, Yeh Hsin-Yi, Chang Ban-Yang
Institute of Biochemistry, National Chung-Hsing University, Taichung 40227, Taiwan.
J Biol Chem. 2007 May 18;282(20):14891-7. doi: 10.1074/jbc.M605177200. Epub 2006 Oct 16.
At initiation of cell division, FtsZ, a tubulin-like GTPase, assembles into a so-called Z-ring structure at the site of division. The formation of Z ring is negatively regulated by EzrA, which ensures only one ring at the midcell per cell cycle. The mechanism leading to the negative regulation of Z-ring formation by EzrA has been analyzed. Our data reveal that the interaction between EzrA and FtsZ not only reduces the GTP-binding ability of FtsZ but also accelerates the rate of GTP hydrolysis, both of which are unfavorable for the polymerization of FtsZ. Moreover, the acceleration in rate of GTP hydrolysis by EzrA is attributed to stabilization of the transition state for GTP hydrolysis and reduction in the affinity of GDP for FtsZ. Clearly, EzrA is able to modify the GTP hydrolysis cycle of FtsZ. On the basis of these results, a model for how EzrA acts to negatively regulate Z-ring formation is proposed.
在细胞分裂开始时,FtsZ(一种微管蛋白样GTP酶)在分裂位点组装成所谓的Z环结构。Z环的形成受到EzrA的负调控,EzrA确保每个细胞周期在细胞中部仅形成一个环。已经分析了EzrA对Z环形成进行负调控的机制。我们的数据表明,EzrA与FtsZ之间的相互作用不仅降低了FtsZ的GTP结合能力,还加速了GTP水解的速率,这两者都不利于FtsZ的聚合。此外,EzrA对GTP水解速率的加速归因于GTP水解过渡态的稳定以及GDP对FtsZ亲和力的降低。显然,EzrA能够改变FtsZ的GTP水解循环。基于这些结果,提出了一个关于EzrA如何对Z环形成进行负调控的模型。