Molecular Basis of Arabidopsis Susceptibility to Pseudomonas Syringae Infection

Michigan State University, East Lansing MI

Investigators

Abstract

In the co-evolution between plants and microbial pathogens, most plants have developed sophisticated defense mechanisms to ward off the majority of (but not all) potential pathogens. When a plant fails to mount a defense response and the pathogen carries appropriate positive virulence factors, disease occurs. In the past decade, significant efforts have been invested in studying how plants defend against pathogens. The use of the Arabidopsis-Pseudomonas syringae pathosystem played a critical role in advancing the understanding of pathogen recognition and plant resistance responses. In contrast, very little is known about how a plant fails to defend itself and ultimately succumbs to infection by virulent pathogens. The goal of this research is to understand the molecular mechanism by which Pseudomonas syringae causes infection in Arabidopsis thaliana. This research is based on the recent finding that the majority of bacterial pathogens of humans, animals, and plants use a specialized protein secretion system (the type III secretion system) to actively "inject" virulence proteins into the host cell. Mutations affecting this pathogen secretion system often eliminate the ability of pathogens to infect the respective hosts, suggesting an important role of "type III virulence proteins" in modulating host susceptibility. However, the molecular mechanisms by which these type III virulence proteins affect host signaling and metabolic processes, which ultimately lead to the establishment of the susceptible interaction, is not understood in any system. In this research, two specific objectives are proposed. The first objective is to link the effects of Pst DC3000 infection to expression of specific Arabidopsis response genes. Successful accomplishment of this objective will remove a major roadblock to progress in the study of susceptible host-bacteria interactions, namely the lack of host cellular and molecular markers. The second objective of this proposal is aimed at achieving a deep understanding of how a specific type III virulence protein, VirPtoB, modulates host susceptibility. Emphasis will be on how VirPtoB, when transgenically expressed inside Arabidopsis leaf cells, alters Arabidopsis gene expression and response to pathogen infection. This research involves the use of genomic, transgenic, and pathogenic methods. Successful completion of this study will contribute to our understanding of those plant cellular mechanisms that must be altered for a plant to become susceptible to pathogens. A postdoctoral student and an undergraduate student will be trained during the course of this research project.