HopW1 from Pseudomonas syringae disrupts the actin cytoskeleton to promote virulence in Arabidopsis.
HopW1 from Pseudomonas syringae disrupts the actin cytoskeleton to promote virulence in Arabidopsis.
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DOI:
10.1371/journal.ppat.1004232
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发表时间:
2014-06
期刊:
影响因子:
6.7
通讯作者:
Greenberg JT
中科院分区:
文献类型:
--
作者:
Kang Y;Jelenska J;Cecchini NM;Li Y;Lee MW;Kovar DR;Greenberg JT
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. Eukaryotic cells require a dynamic actin cytoskeleton for basic functions, some of which are important for immune responses. Such functions include the transport of cellular material to and from different cellular compartments. The plant pathogen Pseudomonas syringae is extracellular and causes disease by injecting effector proteins into plant cells. One of these effectors is HopW1, which disrupts the actin cytoskeleton and reduces the transport of vesicles from the cell surface and proteins destined for vacuoles. The effects of HopW1 can be mimicked using a drug that inhibits actin polymerization. Thus, this work establishes a direct mechanism for pathogen disruption of the actin cytoskeleton and implicates actin-dependent events as important for controlling pathogen growth during infection.
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