Hueck C J
Lehrstuhl für Mikrobiologie, Biozentrum der Universität Würzburg, 97074 Würzburg, Germany.
Microbiol Mol Biol Rev. 1998 Jun;62(2):379-433. doi: 10.1128/MMBR.62.2.379-433.1998.
Various gram-negative animal and plant pathogens use a novel, sec-independent protein secretion system as a basic virulence mechanism. It is becoming increasingly clear that these so-called type III secretion systems inject (translocate) proteins into the cytosol of eukaryotic cells, where the translocated proteins facilitate bacterial pathogenesis by specifically interfering with host cell signal transduction and other cellular processes. Accordingly, some type III secretion systems are activated by bacterial contact with host cell surfaces. Individual type III secretion systems direct the secretion and translocation of a variety of unrelated proteins, which account for species-specific pathogenesis phenotypes. In contrast to the secreted virulence factors, most of the 15 to 20 membrane-associated proteins which constitute the type III secretion apparatus are conserved among different pathogens. Most of the inner membrane components of the type III secretion apparatus show additional homologies to flagellar biosynthetic proteins, while a conserved outer membrane factor is similar to secretins from type II and other secretion pathways. Structurally conserved chaperones which specifically bind to individual secreted proteins play an important role in type III protein secretion, apparently by preventing premature interactions of the secreted factors with other proteins. The genes encoding type III secretion systems are clustered, and various pieces of evidence suggest that these systems have been acquired by horizontal genetic transfer during evolution. Expression of type III secretion systems is coordinately regulated in response to host environmental stimuli by networks of transcription factors. This review comprises a comparison of the structure, function, regulation, and impact on host cells of the type III secretion systems in the animal pathogens Yersinia spp., Pseudomonas aeruginosa, Shigella flexneri, Salmonella typhimurium, enteropathogenic Escherichia coli, and Chlamydia spp. and the plant pathogens Pseudomonas syringae, Erwinia spp., Ralstonia solanacearum, Xanthomonas campestris, and Rhizobium spp.
多种革兰氏阴性动植物病原体利用一种新型的、不依赖Sec的蛋白质分泌系统作为基本的致病机制。越来越清楚的是,这些所谓的III型分泌系统将蛋白质注入(转运)真核细胞的细胞质中,在那里转运的蛋白质通过特异性干扰宿主细胞信号转导和其他细胞过程来促进细菌致病。因此,一些III型分泌系统被细菌与宿主细胞表面的接触所激活。单个III型分泌系统指导多种不相关蛋白质的分泌和转运,这些蛋白质导致了物种特异性的致病表型。与分泌的毒力因子不同,构成III型分泌装置的15至20种膜相关蛋白中的大多数在不同病原体中是保守的。III型分泌装置的大多数内膜成分与鞭毛生物合成蛋白有额外的同源性,而一种保守的外膜因子类似于II型和其他分泌途径的分泌素。特异性结合单个分泌蛋白的结构保守伴侣蛋白在III型蛋白分泌中起重要作用,显然是通过防止分泌因子与其他蛋白过早相互作用来实现的。编码III型分泌系统的基因成簇存在,各种证据表明这些系统是在进化过程中通过水平基因转移获得的。III型分泌系统的表达通过转录因子网络响应宿主环境刺激进行协调调节。本综述比较了动物病原体耶尔森氏菌属、铜绿假单胞菌、福氏志贺菌、鼠伤寒沙门氏菌、肠致病性大肠杆菌和衣原体属以及植物病原体丁香假单胞菌、欧文氏菌属、青枯雷尔氏菌、野油菜黄单胞菌和根瘤菌属中III型分泌系统的结构、功能、调节及其对宿主细胞的影响。