Arp2/3-independent assembly of actin by Vibrio type III effector VopL
Arp2/3-independent assembly of actin by Vibrio type III effector VopL
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DOI：
10.1073/pnas.0703196104
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发表时间：
2007-10-23
影响因子：
11.1
通讯作者：
Orth, Kim
中科院分区：
文献类型：
--
作者：
Liverman, Amy D. B.;Cheng, Hui-Chun;Orth, Kim
微生物病原体在感染期间使用多种机制来破坏肌动蛋白细胞骨架。副溶血性弧菌（Vibrio parahaemolyticus，V.帕拉）是引起胃肠炎的革兰氏阴性细菌，并且新的大流行菌株正在世界各地出现。对副帕拉基因组的分析揭示了III型分泌系统效应子VopL，其编码散布有三个富含脯氨酸的基序的三个Wiskott-Aldrich同源2结构域。用副帕拉感染HeLa细胞以VopL依赖的方式诱导长肌动蛋白纤维的形成。转染VopL促进肌动蛋白应力纤维的组装。在体外，重组VopL有效地诱导组装的肌动蛋白丝生长在其倒刺末端，独立于真核生物的因素。Vibrio VopL被预测为在宿主的肠道感染期间破坏肌动蛋白稳态的细菌毒力因子。
Microbial pathogens use a variety of mechanisms to disrupt the actin cytoskeleton during infection. Vibrio parahaemolyticus (V. para) is a Gram-negative bacterium that causes gastroenteritis, and new pandemic strains are emerging throughout the world. Analysis of the V. para genome revealed a type III secretion system effector, VopL, encoding three Wiskott-Aldrich homology 2 domains that are interspersed with three proline-rich motifs. Infection of HeLa cells with V. para induces the formation of long actin fibers in a VopL-dependent manner. Transfection of VopL promotes the assembly of actin stress fibers. In vitro, recombinant VopL potently induces assembly of actin filaments that grow at their barbed ends, independent of eukaryotic factors. Vibrio VopL is predicted to be a bacterial virulence factor that disrupts actin homeostasis during an enteric infection of the host.