Molecular basis of Arabidopsis susceptibility to Pseudomonas syringae infection

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In the co-evolution between plants and microbial pathogens, most plants have developed sophisticated immune responses to ward off the majority of (but not all) potential pathogens. When a plant fails to defend and the pathogen carries appropriate positive virulence factors, disease occurs. In the past two decades, significant efforts have been invested in studying how plants defend against pathogens at the molecular level. In contrast, little is known about how a plant fails to defend and ultimately succumbs to infection by virulent pathogens. The long-term goal of this project is to contribute to the understanding of the molecular basis of Arabidopsis susceptibility to bacterial pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. Research on susceptible plant-pathogen interactions in the past two decades (mainly from the pathogen side) has revealed a wealth of information about intricate mechanisms used by pathogens to attack host plants. It is now clear that the majority of bacterial pathogens use a specialized protein secretion system-the type III secretion system-to actively 'inject' toxic effector proteins into the host cell. Mutations affecting this protein secretion system eliminate the ability of Pst DC3000 to infect Arabidopsis, suggesting a crucial role of type III effector proteins in modulating Arabidopsis susceptibility. Recent research provides exciting evidence that some type III effector proteins function as inhibitors of various forms of host immunity. For example, effector HopPtoM has recently been shown to inhibit salicylic acid-mediated host basal immunity and, directly or indirectly, to promote host cell death in Arabidopsis. However, the precise mechanisms by which the type III effector proteins modulate host immunity and other host cellular processes are not understood and remain a fundamental question in biology. Molecular genetic, cell biological, genomic, and transgenic experiments described in this grant will identify and characterize Arabidopsis cellular targets of effector HopPtoM. Understanding HopPtoM-mediated suppression of plant immunity and promotion of host cell death likely has broad implications for understanding bacterial pathogenesis in diverse plants. HopPtoM is functionally redundant to another effector, AvrE. Effectors of the HopPtoM and AvrE families are widespread in P. syringae strains and/or other plant-pathogenic bacteria. Most importantly, mutations in the HopPtoM/AvrE families of type III effectors often result in drastic loss of pathogen virulence. Elucidation of the mechanisms by which HopPtoM functions to inactivate the host defenses and to promote host cell death will therefore represent a significant step forward in our understanding of the molecular basis of plant susceptibility to bacterial pathogens. The proposed research also has a broader impact on society. This project will provide training of undergraduate, graduate, and postdoctoral scientists; it will broaden the participation in research of underrepresented groups; it will enhance the PI's teaching activities; and it will enable timely dissemination of knowledge through publications in scientific journals and presentations at regional, national and international conferences and to legislative officers. The basic knowledge gained from this project will provide a foundation for invention of novel strategies for controlling plant diseases, thus improving food quality and yield, reducing use of hazardous chemicals, and increasing national biosecurity and food safety.