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YopR 影响耶尔森氏菌属的 III 型针聚合。

YopR impacts type III needle polymerization in Yersinia species.

机构信息

Department of Microbiology, University of Chicago, Chicago, IL 60637, USA.

出版信息

Mol Microbiol. 2010 Jan;75(1):221-9. doi: 10.1111/j.1365-2958.2009.06988.x. Epub 2009 Dec 7.

Abstract

A hallmark of Yersinia type III machines is the presence of needles extending from the bacterial surface. Needles perform two functions, serving as the conduits for the transport of effectors into immune cells but also acting as a sensor. The polymerized needle protein, YscF, is thought to perceive threshold levels of environmental calcium ions to trigger secretion. yopR (yscH) is a gene downstream of yscEFG, encoding the chaperones and principal building blocks of the needle. Here we investigated the contribution of YopR towards type III secretion and pathogenesis. Yersinia pestis KIM D27 mutants lacking yopR were defective for virulence in a mouse model of septicemic plague. yopR variants of Yersinia enterocolitica W22703 displayed a reduced ability to inject effectors into macrophages and required lower calcium concentrations to activate type III secretion than wild-type yersiniae. Furthermore, yopR mutants failed to assemble YscF into needle complexes and instead secreted YscF into the medium. These results imply that YopR may be involved in controlling the secretion of YscF, thereby impacting the assembly of type III machines. An alternative possibility, which YopR participates directly in the polymerization of YscF, seems less likely as YopR is not associated with purified needles.

摘要

耶尔森氏菌 III 型机器的一个标志是从细菌表面伸出的针。针执行两个功能,作为将效应物输送到免疫细胞的导管,同时也充当传感器。聚合的针蛋白 YscF 被认为可以感知环境钙离子的阈值水平,从而触发分泌。yopR(yscH)是 yscEFG 下游的一个基因,编码针的伴侣和主要构建块。在这里,我们研究了 YopR 对 III 型分泌和发病机制的贡献。鼠疫耶尔森氏菌 KIM D27 突变体缺乏 yopR,在败血症鼠疫的小鼠模型中毒力受损。肠侵袭性大肠杆菌 W22703 的 yopR 变体将效应物注入巨噬细胞的能力降低,并且比野生型耶尔森氏菌激活 III 型分泌所需的钙离子浓度更低。此外,yopR 突变体无法将 YscF 组装成针复合物,而是将 YscF 分泌到培养基中。这些结果表明,YopR 可能参与控制 YscF 的分泌,从而影响 III 型机器的组装。另一种可能性是 YopR 直接参与 YscF 的聚合,但由于 YopR 与纯化的针没有关联,这种可能性似乎不太可能。

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