Campbell-Valois F-X, Pontier Stéphanie M
Department of Chemistry and Biomolecular Sciences, University of Ottawa Ottawa, ON, Canada.
Independent Researcher Ottawa, ON, Canada.
Front Cell Infect Microbiol. 2016 Mar 9;6:28. doi: 10.3389/fcimb.2016.00028. eCollection 2016.
Shigella spp. are Gram-negative bacterial pathogens that infect human colonic epithelia and cause bacterial dysentery. These bacteria express multiple copies of a syringe-like protein complex, the Type Three Secretion apparatus (T3SA), which is instrumental in the etiology of the disease. The T3SA triggers the plasma membrane (PM) engulfment of the bacteria by host cells during the initial entry process. It then enables bacteria to escape the resulting phagocytic-like vacuole. Freed bacteria form actin comets to move in the cytoplasm, which provokes bacterial collision with the inner leaflet of the PM. This phenomenon culminates in T3SA-dependent secondary uptake and vacuolar rupture in neighboring cells in a process akin to what is observed during entry and named cell-to-cell spread. The activity of the T3SA of Shigella flexneri was recently demonstrated to display an on/off regulation during the infection. While the T3SA is active when bacteria are in contact with PM-derived compartments, it switches to an inactive state when bacteria are released within the cytosol. These observations indicate that effector proteins transiting through the T3SA are therefore translocated in a highly time and space constrained fashion, likely impacting on their cellular distribution. Herein, we present what is currently known about the composition, the assembly and the regulation of the T3SA activity and discuss the consequences of the on/off regulation of T3SA on Shigella effector properties and functions during the infection. Specific examples that will be developed include the role of effectors IcsB and VirA in the escape from LC3/ATG8-positive vacuoles formed during cell-to-cell spread and of IpaJ protease activity against N-miristoylated proteins. The conservation of a similar regulation of T3SA activity in other pathogens such as Salmonella or Enteropathogenic Escherichia coli will also be briefly discussed.
志贺氏菌属是革兰氏阴性细菌病原体,可感染人类结肠上皮并引起细菌性痢疾。这些细菌表达多拷贝的注射器样蛋白复合物——三型分泌装置(T3SA),该装置在疾病病因学中起重要作用。在初始进入过程中,T3SA触发宿主细胞对细菌的质膜(PM)吞噬。然后,它使细菌能够逃离由此形成的吞噬样液泡。释放出的细菌形成肌动蛋白彗星样结构在细胞质中移动,这引发细菌与质膜内小叶的碰撞。这一现象最终导致T3SA依赖的二次摄取和邻近细胞中的液泡破裂,这一过程类似于在进入过程中观察到的情况,被称为细胞间传播。最近证明,福氏志贺氏菌的T3SA活性在感染过程中表现出开/关调节。当细菌与源自质膜的区室接触时,T3SA处于活跃状态,而当细菌在胞质溶胶中释放时,它会切换到非活跃状态。这些观察结果表明,通过T3SA转运的效应蛋白因此以高度受时间和空间限制的方式转运,这可能会影响它们在细胞内的分布。在此,我们介绍目前已知的T3SA活性的组成、组装和调节,并讨论T3SA的开/关调节对志贺氏菌效应蛋白特性和感染期间功能的影响。将阐述的具体例子包括效应蛋白IcsB和VirA在细胞间传播过程中从LC3/ATG8阳性液泡逃逸中的作用,以及IpaJ蛋白酶对N-豆蔻酰化蛋白的活性。还将简要讨论其他病原体如沙门氏菌或肠致病性大肠杆菌中T3SA活性的类似调节的保守性。