Chlamydia trachomatis is the leading cause of infectious blindness and a sexually transmitted infection. All chlamydiae are obligate intracellular bacteria that replicate within a membrane-bound vacuole termed the inclusion. From the confines of the inclusion, the bacteria must interact with many host organelles to acquire key nutrients necessary for replication, all while promoting host cell viability and subverting host defense mechanisms. To achieve these feats, C. trachomatis delivers an arsenal of virulence factors into the eukaryotic cell via a type 3 secretion system (T3SS) that facilitates invasion, manipulation of host vesicular trafficking, subversion of host defense mechanisms and promotes bacteria egress at the conclusion of the developmental cycle. A subset of these proteins intercalate into the inclusion and are thus referred to as inclusion membrane proteins. Whereas others, referred to as conventional T3SS effectors, are released into the host cell where they localize to various eukaryotic organelles or remain in the cytosol. Here, we discuss the functions of T3SS effector proteins with a focus on how advances in chlamydial genetics have facilitated the identification and molecular characterization of these important factors.

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有变种人吗？衣原体遗传学的进步如何进一步推进效应蛋白的研究

沙眼衣原体是导致传染性失明和性传播感染的主要原因。所有衣原体都是专性细胞内细菌，在称为包涵体的膜结合液泡内复制。从内含物的范围来看，细菌必须与许多宿主细胞器相互作用，以获得复制所需的关键营养物质，同时促进宿主细胞活力并破坏宿主防御机制。为了实现这些壮举，沙眼衣原体通过 3 型分泌系统 (T3SS) 将毒力因子库输送到真核细胞中，促进入侵、操纵宿主囊泡运输、颠覆宿主防御机制并在结束时促进细菌流出。发育周期。这些蛋白质的一个子集嵌入到包涵体中，因此被称为包涵体膜蛋白。而其他被称为传统 T3SS 效应器的效应器则被释放到宿主细胞中，定位到各种真核细胞器或保留在细胞质中。在这里，我们讨论 T3SS 效应蛋白的功能，重点讨论衣原体遗传学的进步如何促进这些重要因子的识别和分子表征。