Kang Yongsung, Jelenska Joanna, Cecchini Nicolas M, Li Yujie, Lee Min Woo, Kovar David R, Greenberg Jean T
Department of Molecular Genetics and Cell Biology, The University of Chicago, Chicago, Illinois, United States of America.
PLoS Pathog. 2014 Jun 26;10(6):e1004232. doi: 10.1371/journal.ppat.1004232. eCollection 2014 Jun.
A central mechanism of virulence of extracellular bacterial pathogens is the injection into host cells of effector proteins that modify host cellular functions. HopW1 is an effector injected by the type III secretion system that increases the growth of the plant pathogen Pseudomonas syringae on the Columbia accession of Arabidopsis. When delivered by P. syringae into plant cells, HopW1 causes a reduction in the filamentous actin (F-actin) network and the inhibition of endocytosis, a known actin-dependent process. When directly produced in plants, HopW1 forms complexes with actin, disrupts the actin cytoskeleton and inhibits endocytosis as well as the trafficking of certain proteins to vacuoles. The C-terminal region of HopW1 can reduce the length of actin filaments and therefore solubilize F-actin in vitro. Thus, HopW1 acts by disrupting the actin cytoskeleton and the cell biological processes that depend on actin, which in turn are needed for restricting P. syringae growth in Arabidopsis.
细胞外细菌病原体致病的一个核心机制是向宿主细胞注射能够改变宿主细胞功能的效应蛋白。HopW1是一种由III型分泌系统注射的效应蛋白，它能促进植物病原体丁香假单胞菌在拟南芥哥伦比亚生态型上的生长。当由丁香假单胞菌递送到植物细胞中时，HopW1会导致丝状肌动蛋白（F-肌动蛋白）网络减少并抑制内吞作用，这是一个已知的肌动蛋白依赖性过程。当在植物中直接产生时，HopW1与肌动蛋白形成复合物，破坏肌动蛋白细胞骨架并抑制内吞作用以及某些蛋白质向液泡的运输。HopW1的C末端区域可以缩短肌动蛋白丝的长度，因此在体外可溶解F-肌动蛋白。因此，HopW1通过破坏肌动蛋白细胞骨架和依赖于肌动蛋白的细胞生物学过程来发挥作用，而这些过程反过来又是限制丁香假单胞菌在拟南芥中生长所必需的。
