Helmholtz Centre for Infection Research, Braunschweig, Germany.
Cell Microbiol. 2010 Jan;12(1):84-98. doi: 10.1111/j.1462-5822.2009.01380.x. Epub 2009 Sep 2.
Type III secretion system-mediated injection of a cocktail of bacterial proteins drives actin rearrangements, frequently adopting the shape of prominent protuberances of ruffling membrane, and culminating in host cell invasion of Gram-negative pathogens like Salmonella typhimurium. Different Salmonella effectors are able to bind actin and activate Rho-family GTPases, which have previously been implicated in mediating actin-dependent Salmonella entry by interacting with N-WASP or WAVE-complex, well-established activators of the actin nucleation machine Arp2/3-complex. Using genetic deletion and RNA interference studies, we show here that neither individual nor collective removal of these Arp2/3- complex activators affected host cell invasion as efficiently as Arp2/3-complex knock-down, although the latter was also not essential. However, interference with WAVE-complex function abrogated Salmonella-induced membrane ruffling without significantly affecting entry efficiency, actin or Arp2/3-complex accumulation. In addition, scanning electron microscopy images captured entry events in the absence of prominent membrane ruffles. Finally, localization and RNA interference studies indicated a relevant function in Salmonella entry for the novel Arp2/3-complex regulator WASH. These data establish for the first time that Salmonella invasion is separable from bacteria-induced membrane ruffling, and uncover an additional Arp2/3-complex activator as well as an Arp2/3-complex-independent actin assembly activity that contribute to Salmonella invasion.
III 型分泌系统介导的细菌蛋白混合物注射会导致肌动蛋白重排,通常会形成明显的皱褶膜突起形状,并最终导致革兰氏阴性病原体(如鼠伤寒沙门氏菌)侵入宿主细胞。不同的沙门氏菌效应物能够结合肌动蛋白并激活 Rho 家族 GTPases,这些 GTPases 先前被认为通过与 N-WASP 或 WAVE 复合物相互作用,介导肌动蛋白依赖性沙门氏菌进入,而 N-WASP 或 WAVE 复合物是 Arp2/3 复合物这一公认的肌动蛋白成核机器的激活剂。通过遗传缺失和 RNA 干扰研究,我们在这里表明,单个或集体去除这些 Arp2/3 复合物激活剂并不像 Arp2/3 复合物敲低那样有效地影响宿主细胞入侵,尽管后者也不是必需的。然而,干扰 WAVE 复合物的功能会破坏沙门氏菌诱导的细胞膜皱褶,而不会显著影响进入效率、肌动蛋白或 Arp2/3 复合物的积累。此外,扫描电子显微镜图像捕捉到在没有明显细胞膜皱褶的情况下的进入事件。最后,定位和 RNA 干扰研究表明,新型 Arp2/3 复合物调节剂 WASH 在沙门氏菌进入中具有相关功能。这些数据首次确立了沙门氏菌入侵与细菌诱导的细胞膜皱褶是可分离的,并揭示了一种额外的 Arp2/3 复合物激活剂以及一种 Arp2/3 复合物独立的肌动蛋白组装活性,它们有助于沙门氏菌入侵。