Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan 48105, USA.
J Biol Chem. 2011 Mar 25;286(12):10378-86. doi: 10.1074/jbc.M110.167031. Epub 2011 Jan 5.
EpsE is an ATPase that powers transport of cholera toxin and hydrolytic enzymes through the Type II secretion (T2S) apparatus in the gram-negative bacterium, Vibrio cholerae. On the basis of structures of homologous Type II/IV secretion ATPases and our biochemical data, we believe that EpsE is active as an oligomer, likely a hexamer, and the binding, hydrolysis, and release of nucleotide cause EpsE to undergo dynamic structural changes, thus converting chemical energy to mechanical work, ultimately resulting in extracellular secretion. The conformational changes that occur as a consequence of nucleotide binding would realign conserved arginines (Arg(210), Arg(225), Arg(320), Arg(324), Arg(336), and Arg(369)) from adjoining domains and subunits to complete the active site around the bound nucleotide. Our data suggest that these arginines are essential for ATP hydrolysis, although their roles in shaping the active site of EpsE are varied. Specifically, we have shown that replacements of these arginine residues abrogate the T2S process due to a reduction of ATPase activity yet do not have any measurable effect on nucleotide binding or oligomerization of EpsE. We have further demonstrated that point mutations in the EpsE intersubunit interface also reduce ATPase activity without disrupting oligomerization, strengthening the idea that residues from multiple subunits must precisely interact in order for EpsE to be sufficiently active to support T2S. Our findings suggest that the action of EpsE is similar to that of other Type II/IV secretion ATPase family members, and thus these results may be widely applicable to the family as a whole.
EpsE 是一种 ATP 酶,可在革兰氏阴性霍乱弧菌的 II 型分泌(T2S)装置中为霍乱毒素和水解酶的转运提供动力。基于结构同源的 II 型/IV 型分泌 ATP 酶和我们的生化数据,我们相信 EpsE 作为一个寡聚体(可能是六聚体)发挥作用,核苷酸的结合、水解和释放导致 EpsE 发生动态结构变化,从而将化学能转化为机械能,最终导致细胞外分泌。核苷酸结合引起的构象变化会重新排列相邻结构域和亚基中的保守精氨酸(Arg(210)、Arg(225)、Arg(320)、Arg(324)、Arg(336)和 Arg(369))以完成结合核苷酸周围的活性位点。我们的数据表明,这些精氨酸对于 ATP 水解至关重要,尽管它们在塑造 EpsE 的活性位点方面的作用有所不同。具体来说,我们已经表明,这些精氨酸残基的替换会由于 ATP 酶活性的降低而使 T2S 过程受阻,但对核苷酸结合或 EpsE 的寡聚化没有任何可测量的影响。我们进一步证明,EpsE 亚基间界面的点突变也会降低 ATP 酶活性而不破坏寡聚化,这进一步表明,来自多个亚基的残基必须精确相互作用,以使 EpsE 具有足够的活性来支持 T2S。我们的研究结果表明,EpsE 的作用类似于其他 II 型/IV 型分泌 ATP 酶家族成员,因此这些结果可能广泛适用于整个家族。