Department of Molecular and Cellular Biology, University of Guelph, Guelph, Ontario N1G 2W1, Canada.
J Biol Chem. 2012 Oct 26;287(44):37030-41. doi: 10.1074/jbc.M112.397612. Epub 2012 Sep 11.
The mono-ADP-ribosyltransferase (mART) toxins are contributing factors to a number of human diseases, including cholera, diphtheria, traveler's diarrhea, and whooping cough. VahC is a cytotoxic, actin-targeting mART from Aeromonas hydrophila PPD134/91. This bacterium is implicated primarily in diseases among freshwater fish species but also contributes to gastrointestinal and extraintestinal infections in humans. VahC was shown to ADP-ribosylate Arg-177 of actin, and the kinetic parameters were K(m)(NAD(+)) = 6 μM, K(m)(actin) = 24 μM, and k(cat) = 22 s(-1). VahC activity caused depolymerization of actin filaments, which induced caspase-mediated apoptosis in HeLa Tet-Off cells. Alanine-scanning mutagenesis of predicted catalytic residues showed the predicted loss of in vitro mART activity and cytotoxicity. Bioinformatic and kinetic analysis also identified three residues in the active site loop that were critical for the catalytic mechanism. A 1.9 Å crystal structure supported the proposed roles of these residues and their conserved nature among toxin homologues. Several small molecules were characterized as inhibitors of in vitro VahC mART activity and suramin was the best inhibitor (IC(50) = 20 μM). Inhibitor activity was also characterized against two other actin-targeting mART toxins. Notably, these inhibitors represent the first report of broad spectrum inhibition of actin-targeting mART toxins.
单 ADP- 核糖基转移酶 (mART) 毒素是许多人类疾病的致病因素,包括霍乱、白喉、旅行者腹泻和百日咳。VahC 是一种来自气单胞菌属的细胞毒性、肌动蛋白靶向 mART。这种细菌主要与淡水鱼类疾病有关,但也会导致人类胃肠道和肠道外感染。研究表明,VahC 可以将 ADP- 核糖基转移到肌动蛋白的 Arg-177 上,动力学参数为 K(m)(NAD(+)) = 6 μM,K(m)(肌动蛋白) = 24 μM,k(cat) = 22 s(-1)。VahC 活性导致肌动蛋白丝的解聚,从而诱导 HeLa Tet-Off 细胞中 caspase 介导的细胞凋亡。对预测催化残基的丙氨酸扫描突变显示,体外 mART 活性和细胞毒性丧失。生物信息学和动力学分析还确定了活性位点环中的三个残基对催化机制至关重要。1.9 Å 的晶体结构支持了这些残基的作用及其在毒素同源物中的保守性质。几种小分子被鉴定为体外 VahC mART 活性的抑制剂,苏拉明是最好的抑制剂 (IC(50) = 20 μM)。抑制剂活性也针对另外两种靶向肌动蛋白的 mART 毒素进行了表征。值得注意的是,这些抑制剂代表了对靶向肌动蛋白的 mART 毒素的广谱抑制作用的首次报道。