Meet the Faculty

Walter Gassmann

Associate Professor
Division of Plant Sciences

Phone: 573-884-7703
Fax: 573-884-9676
E-mail: GassmannW@missouri.edu
Address: 371C Life Sciences Center

Education
M.S., Biochemistry, Swiss Federal Institute of Technology, Switzerland
Ph.D., Biology, University of California, San Diego

Description
Plants are continuously exposed to potential pathogens, yet most plants are resistant to most pathogens. Plants have evolved a surveillance system with similarities to the innate immune system of animals that detects invading pathogens.

Specifically, plants express a large number of resistance genes that, directly or indirectly, interact with effector proteins of pathogens and trigger a plant disease resistance response. Pathogens in turn evolve to overcome this resistance, either by deleting or altering the detected effector proteins or directly counteracting the plant response.

The co-evolution of host and pathogen is evident in the large number of pathogen strains within a given species expressing specific effector proteins, and in the large number of plant disease resistance genes. It is estimated that Arabidopsis has devoted more than one percent of its genome just to resistance genes.

Gene-for-gene resistance conferred by the A. thaliana RPS4 gene. Leaves were inoculated with Pseudomonas syringae. Disease (chlorosis) occurs when the host resistance gene (left column) or the pathogen avirulence gene (top row) is absent. Resistance only ensues when both genes are present (bottom right).

Walter Gassman's research is aimed at understanding the function of this important class of plant genes. He and his colleagues are focusing on the Arabidopsis RPS4 gene specifying resistance to Pseudomonas syringae expressing the cognate avirulence gene avrRps4.

They recently isolated RPS4 by map-based cloning and determined that it belongs to the TIR-NBS-LRR class of plant disease resistance genes. This class shows homology at the N-terminus of the predicted protein to known proteins involved in the animal innate immune response.

Because avrRps4 constitutes the only cloned avirulence gene for an Arabidopsis TIR-NBS-LRR resistance gene, this system will allow the researchers a detailed analysis of the TIR-NBS-LRR gene-dependent disease resistance signaling pathway. This involves structure/function analyses of the RPS4 gene product as well as genetic screens of randomly mutagenized Arabidopsis plants for mutants in the RPS4 signaling pathway.

For example, the lab has isolated mutants in the naturally avrRps4-susceptible Arabidopsis accession RLD that are now specifically resistant to bacteria expressing avrRps4, but do not show general enhanced resistance. These mutants may define novel loci in the RPS4 signaling pathway that would not be identified in loss-of-resistance screens.

Further, they are studying the A. thaliana disease resistance response using electrophysiological techniques. They have identified a pattern of membrane depolarization that precedes plant defense-related cell death.