Rho-dependent membrane folding causes Shigella entry into epithelial cells
Rho-dependent membrane folding causes Shigella entry into epithelial cells
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DOI：
10.1002/j.1460-2075.1996.tb00696.x
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发表时间：
1996-07-01
期刊：
影响因子：
11.4
通讯作者：
Sansonetti, P
中科院分区：
文献类型：
--
作者：
Adam, T;Giry, M;Sansonetti, P
小的GT_rho在功能上参与细胞骨架结构如应力纤维或粘着斑的形成。志贺氏菌进入HeLa细胞诱导在细菌进入位点处的花状膜结构。我们在这里表明，这种膜折叠过程是rho依赖的。三种rho亚型被招募到细菌进入位点，相对于膜结构具有差异定位。rho特异性抑制剂消除志贺氏菌诱导的膜折叠，并相应地损害细菌进入。S1-肌球蛋白标记表明，rho参与志贺氏菌诱导的肌动蛋白聚合，但不肌动蛋白成核的细菌入侵网站。这提供了允许细菌病原体进入真核细胞的信号级联中的主要环节。
The small GTPase rho is functionally involved in the formation of cytoskeletal structures like stress fibers or focal adhesion plaques. Shigella entry into HeLa cells induces a blossom-like membrane structure at the bacterial entry site. We show here that this membrane-folding process is rho-dependent. The three rho isoforms were recruited into bacterial entry sites with differential localization relative to the membrane structure. A rho-specific inhibitor abolished Shigella-induced membrane folding and impaired bacterial entry accordingly. S1-myosin labeling indicated that rho was involved in Shigella-induced actin polymerization but not actin nucleation in the bacterial invasion site. This provides a major link in the signalization cascade allowing entry of a bacterial pathogen into a eukaryotic cell.