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首页> 外文期刊>Infection and immunity >EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization
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EseG, an Effector of the Type III Secretion System of Edwardsiella tarda, Triggers Microtubule Destabilization

机译：EseG，爱德华氏菌III型分泌系统的效应物，触发微管失稳

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Edwardsiella tarda is a Gram-negative enteric pathogen that causes hemorrhagic septicemia in fish and both gastrointestinal and extraintestinal infections in humans. A type III secretion system (T3SS) was recently shown to contribute to pathogenesis, since deletions of various T3SS genes increased the 50% lethal dose (LD50) by about 1 log unit in the blue gourami infection model. In this study, we report EseG as the first identified effector protein of T3SS. EseG shares partial homology with two Salmonella T3SS effectors (SseG and SseF) over a conserved domain (amino acid residues 142 to 192). The secretion of EseG is dependent on a functional T3SS and, in particular, requires the chaperone EscB. Experiments using TEM-1 β-lactamase as a fluorescence-based reporter showed that EseG was translocated into HeLa cells at 35°C. Fractionation of infected HeLa cells demonstrated that EseG was localized to the host membrane fraction after translocation. EseG is able to disassemble microtubule structures when overexpressed in mammalian cells. This phenotype may require a conserved motif of EseG (EseG142-192), since truncated versions of EseG devoid of this motif lose their ability to cause microtubule destabilization. By demonstrating the function of EseG, our study contributes to the understanding of E. tarda pathogenesis. Moreover, the approach established in this study to identify type III effectors can be used to identify and characterize more type III and possible type VI effectors in Edwardsiella.
机译： Edwardsiella tarda 是革兰氏阴性肠病原体，可导致鱼类出血性败血病以及人类的胃肠道和肠外感染。最近发现，III型分泌系统（T3SS）促成发病机理，因为在蓝色钩吻菌感染模型中，各种T3SS基因的缺失使50％致死剂量（LD 50 ）的致死剂量增加了约1个对数单位。在这项研究中，我们报告EseG是T3SS的第一个鉴定的效应蛋白。 EseG与两个 Salmonella T3SS效应子（SseG和SseF）在保守域（氨基酸残基142至192）上具有部分同源性。 EseG的分泌取决于功能性T3SS，特别是需要伴侣EscB。使用TEM-1β-内酰胺酶作为基于荧光的报告基因的实验表明，EseG在35°C时易位到HeLa细胞中。感染的HeLa细胞的分级分离表明，易位后EseG定位于宿主膜级分。当在哺乳动物细胞中过度表达时，EseG能够分解微管结构。此表型可能需要EseG的保守基序（EseG 142-192 ），因为缺少该基序的EseG的截短形式会失去引起微管不稳定的能力。通过展示EseG的功能，我们的研究有助于对 E的理解。 tarda 的发病机理。此外，在这项研究中建立的识别III型效应子的方法可用于鉴定和鉴定 Edwardsiella 中更多的III型和可能的VI型效应子。

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