Interactions between plant pathogens and their hosts are highly specific, suggesting that plant-pathogen interactions involve a continual exchange of informatin between the two organisms. For example, initiation of pathogenic interactions is dependent on the pathogen's ability to recognize, invade and grow in suitable host plants. Super-imposed on the establishment of these interactions is the potential for the host plant to detect the presence of a specific pathogen and, as a result of this pathogen re cognition event, rapidly induce expression of a resistance response. The three major questions that our research focuses on are: 1) What is the molecular basis of pathogenicity? 2) What are the mechanisms governing plant pathogen recognition? and 3) How does pathogen recognition result in the induction of plant defense responses? In order to address these questions we are studying the interaction between Arabidopsis thaliana and the bacterial pathogen Pseudomonas syringae, a system in wh ich both plant and pathogen are amenable to genetic and molecular analyses.
We are using genetic and molecular approaches to identify and characterize plant genes that control pathogen recognition and the subsequent expression of disease resistance. Mutational analyses of resistance in Arabidopsis to P. syringae ha s resulted in the identification of susceptible mutants, including several that define a locus, RPS2, that is required for pathogen recognition. The RPS2 locus has recently been cloned, and sequence analysis revealed several motifs that sug est that the RPS2 protein may interact with other protein components of the cell. However, the role of this protein in mediating disease resistance still remains unclear. One of the focuses of my laboratory is to further characterize the RPS2 loc us and to study its role in disease resistance. This project includes molecular and biochemical studies designed to address how RPS2 mediates recognitional specificity and identify other components of the defense response pathway. Additional plan t genes required for disease resistance are being identified by employing several different genetic stategies, including characterizing additional susceptible mutants and screening for suppressors and enhancers of the rps2 mutant phenotype.
My laboratory is also using a combination of approaches to study pathogenicity in P. syringae. One approach involves the positive selection for bacterial genes that are specifically induced in planta. The functional role of these genes in
disease development will then be tested by reverse genetic techniques. A complementary gentic approach involves the isolation and characterization of P. syringae mutants that are no longer able to cause disease on Arabidopsis.