Scholar Profile

Barbara N. Kunkel

Professor
Department of Biology
Washington University
One North Brookings Drive
Campus Box 1137
St. Louis, MO 63130
Voice: 314-935-7284
Fax: 314-935-4432
Email: kunkel@biodec.wustl.edu
Personal Homepage
1996 Searle Scholar

Research Interests

Plant-pathogen interactions

Interactions between plant pathogens and their hosts are highly specific; most plant pathogens are able to infect and cause disease on only one or a small number of host species. This specificity suggests that recognition mechanisms govern plant-pathogen interactions and that molecular signals passing between pathogen and host determine whether such interactions result in disease or resistance. For example, initiation of a pathogenic interaction is dependent on the pathogen's ability to recognize, invade and grow in a suitable host (Fig. 1). Super-imposed on the establishment of such an interaction is the potential for the host plant to detect the presence of a specific pathogen and, as a result of this pathogen recognition event, rapidly induce expression of a resistance response (Fig. 2). Three of the fundamental questions that I would like to address in my research program over the next several years are: 1) What is the molecular basis of pathogenicity in plant pathogens? 2) What are the mechanisms governing plant-pathogen recognition? 3) How does pathogen recognition result in the induction of plant defense responses?

In order to address these issues I have chosen to study the interaction between the bacterial pathogen Pseudomonas syringae and one of its plant hosts, Arabidopsis thaliana, a system in which both pathogen and host are amenable to genetic and molecular analysis. Currently my research group is using a variety of molecular genetic approaches to identify and characterize both pathogen and plant genes that govern the interactions between these two organisms.

 

Molecular genetic basis of pathogenicity in P. syringae.

To gain a better understanding of the mechanisms governing pathogenicity in P. syringae, we are using a variety of approaches to identify and characterize bacterial genes that are involved in pathogenesis. One approach involves screening for P. syringae mutants that no longer cause disease on Arabidopsis. This screen has been designed to identify genes that are involved in all steps of pathogenesis, including determination of host specificity, epiphytic survival, entry into plant tissue, acquisition and utilization of nutrients, evasion and/or suppression of host defense responses, tissue damage and the production of disease symptoms.

A complementary molecular approach is based on the in vivo expression technology (IVET) system developed by Mahan et al (1993; Science 259: 686-688). This approach, which is based on the expectation that a large number of pathogen genes that are expressed specifically during the infection process are important for pathogenesis, involves positive selection for bacterial genes that are specifically induced upon infection of the plant. The functional role of these genes in pathogenesis will then be tested by reverse genetic techniques.

 

Identification of plant genes involved in resistance

Mutational analyses of resistance in Arabidopsis to P. syringae has resulted in the identification of a locus, RPS2, that is required for pathogen recognition. The predicted RPS2 protein product contains several motifs, including a series of leucine-rich repeats (LRR), that suggest that RPS2 may interact with other protein components of the cell, perhaps as a component of a signal transduction pathway linking pathogen recognition to the activation of plant defense responses. We are now further characterizing RPS2 and its role in disease resistance. These studies include molecular and biochemical experiments designed to address how RPS2 mediates recognitional specificity, as well as genetic experiments aimed at identifying other components of the defense response pathway. We hope to identify additional plant genes required for disease resistance by screening for suppressors and enhancers of mutant lines carrying defective RPS2 alleles, as well as by characterizing additional previously identified susceptible plant lines. These studies should lead to the identification of genes encoding cellular components that interact directly with RPS2, genes controlling signal transduction events downstream of pathogen recognition, and genes whose products may play a direct role in the defense response.

The identification and characterization of both bacterial genes governing pathogenicity and plant genes controlling pathogen recognition and the expression of disease resistance will contribute to our understanding of the complex signaling events that mediate plant-pathogen interactions.