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The Pseudomonas syringae Type III Effector HopAM1 Enhances Virulence on Water-Stressed Plants

March 2008 , Volume 21 , Number  3
Pages  361 - 370

Ajay K. Goel,1 Derek Lundberg,1,2 Miguel A. Torres,1 Ryan Matthews,1 Chiharu Akimoto-Tomiyama,1 Lisa Farmer,3 Jeffery L. Dangl,1,2,4,5 and Sarah R. Grant1,2

1Department of Biology and 2Curriculum in Genetics and Molecular Biology, University of North Carolina at Chapel Hill, Chapel Hill 27599, U.S.A.; 3Department of Horticulture and Cellular and Molecular Biology, 1575 Linden Drive, University of Wisconsin-Madison, Madison 53706, U.S.A.; 4Department of Microbiology and Immunology and 5Carolina Center for Genome Sciences, University of North Carolina at Chapel Hill, U.S.A.


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Accepted 29 October 2007.

Pseudomonas syringae strains deliver diverse type III effector proteins into host cells, where they can act as virulence factors. Although the functions of the majority of type III effectors are unknown, several have been shown to interfere with plant basal defense mechanisms. Type III effectors also could contribute to bacterial virulence by enhancing nutrient uptake and pathogen adaptation to the environment of the host plant. We demonstrate that the type III effector HopAM1 (formerly known as AvrPpiB) enhances the virulence of a weak pathogen in plants that are grown under drought stress. This is the first report of a type III effector that aids pathogen adaptation to water availability in the host plant. Expression of HopAM1 makes transgenic Ws-0 Arabidopsis hypersensitive to abscisic acid (ABA) for stomatal closure and germination arrest. Conditional expression of HopAM1 in Arabidopsis also suppresses basal defenses. ABA responses overlap with defense responses and ABA has been shown to suppress defense against P. syringae pathogens. We propose that HopAM1 aids P. syringae virulence by manipulation of ABA responses that suppress defense responses. In addition, host ABA responses enhanced by type III delivery of HopAM1 protect developing bacterial colonies inside leaves from osmotic stress.



© 2008 The American Phytopathological Society