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Plant Physiol. 2016 Jul;171(3):2239-55. doi: 10.1104/pp.16.01593. Epub 2016 May 23.

The Pseudomonas syringae Type III Effector HopG1 Induces Actin Remodeling to Promote Symptom Development and Susceptibility during Infection.

Author information

1
Department of Plant, Soil and Microbial Sciences, Michigan State University, East Lansing, Michigan 48824 (M.S., Y.-J.L., B.D.); Graduate Program in Cell and Molecular Biology, Michigan State University, East Lansing, Michigan 48824 (K.P., S.Y.H., B.D.); Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824 (B.H.K., S.Y.H.); Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-2064 (J.H.-R., C.J.S.); Department of Botany and Plant Pathology, Oregon State University, Corvallis, Oregon 97331-7303 (A.C., J.H.C.);Molecular and Cellular Biology Program, Oregon State University, Corvallis, Oregon 97331-7303 (A.C., J.H.C.);Howard Hughes Medical Institute and the Gordon and Betty Moore Foundation, Michigan State University, East Lansing, Michigan 48824 (S.Y.H.); Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon 97331-7303 (J.H.C.);Bindley Bioscience Center, Discovery Park, Purdue University, West Lafayette, Indiana 47907 (C.J.S.); and Graduate Program in Genetics, Michigan State University, East Lansing, Michigan 48824 (B.D.).
2
Department of Plant, Soil and Microbial Sciences, Michigan State University, East Lansing, Michigan 48824 (M.S., Y.-J.L., B.D.); Graduate Program in Cell and Molecular Biology, Michigan State University, East Lansing, Michigan 48824 (K.P., S.Y.H., B.D.); Department of Energy Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824 (B.H.K., S.Y.H.); Department of Biological Sciences, Purdue University, West Lafayette, Indiana 47907-2064 (J.H.-R., C.J.S.); Department of Botany and Plant Pathology, Oregon State University, Corvallis, Oregon 97331-7303 (A.C., J.H.C.);Molecular and Cellular Biology Program, Oregon State University, Corvallis, Oregon 97331-7303 (A.C., J.H.C.);Howard Hughes Medical Institute and the Gordon and Betty Moore Foundation, Michigan State University, East Lansing, Michigan 48824 (S.Y.H.); Center for Genome Research and Biocomputing, Oregon State University, Corvallis, Oregon 97331-7303 (J.H.C.);Bindley Bioscience Center, Discovery Park, Purdue University, West Lafayette, Indiana 47907 (C.J.S.); and Graduate Program in Genetics, Michigan State University, East Lansing, Michigan 48824 (B.D.) bday@msu.edu.

Abstract

The plant cytoskeleton underpins the function of a multitude of cellular mechanisms, including those associated with developmental- and stress-associated signaling processes. In recent years, the actin cytoskeleton has been demonstrated to play a key role in plant immune signaling, including a recent demonstration that pathogens target actin filaments to block plant defense and immunity. Herein, we quantified spatial changes in host actin filament organization after infection with Pseudomonas syringae pv. tomato DC3000 (Pst DC3000), demonstrating that the type-III effector HopG1 is required for pathogen-induced changes to actin filament architecture and host disease symptom development during infection. Using a suite of pathogen effector deletion constructs, coupled with high-resolution microscopy, we found that deletion of hopG1 from Pst DC3000 resulted in a reduction in actin bundling and a concomitant increase in the density of filament arrays in Arabidopsis, both of which correlate with host disease symptom development. As a mechanism underpinning this activity, we further show that the HopG1 effector interacts with an Arabidopsis mitochondrial-localized kinesin motor protein. Kinesin mutant plants show reduced disease symptoms after pathogen infection, which can be complemented by actin-modifying agents. In total, our results support a model in which HopG1 induces changes in the organization of the actin cytoskeleton as part of its virulence function in promoting disease symptom development.

PMID:
27217495
PMCID:
PMC4936540
DOI:
10.1104/pp.16.01593
[Indexed for MEDLINE]
Free PMC Article

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