My research focuses on bacterial speck disease which is caused by the infection of tomato leaves by the bacterial pathogen Pseudomonas syringae pv. tomato. This is an economically important disease that can decrease both the yield and quality of tomato fruits. It also serves as an excellent model system for understanding plant-pathogen biology because much is known about the molecular biology of this pathosystem and many genomics resources are available for both tomato and P. s. pv. tomato.|In the tomato-Pseudomonas interaction, the virulence proteins AvrPto and AvrPtoB are delivered into the plant cell by the bacterial type III secretion system. Both proteins then act to suppress host basal defenses and thereby promote plant disease susceptibility. Some tomato genotypes express the Pto gene which encodes a protein kinase that detects the presence of AvrPto and AvrPtoB and confers resistance to bacterial speck disease. This resistance is activated by the physical interaction of the Pto kinase with AvrPto or AvrPtoB and also by the interaction of Pto with Prf, a protein containing a nucleotide-binding site and a region of leucine-rich repeats (i.e., an NB-LRR protein). This early recognition event activates a complex series of signaling events that leads ultimately to host defense responses, including transcriptional reprogramming and localized host cell death, that restrict growth of the pathogen. We have found recently that a C-terminal domain of AvrPtoB encodes an E3 ubiquitin ligase that, in certain tomato genotypes, can interfere with activation of this host resistance response. Thus, some bacterial virulence proteins appear to have evolved to suppress both basal and resistance-gene mediated host defenses and plants have, in turn, evolved to interfere with both of these activities.|To further understand the molecular basis of bacterial virulence, plant immunity, and susceptibility in this pathosystem we are using various experimental approaches including: genomics, biochemistry, cell biology, molecular biology, forward and reverse genetics, and structural biology. ||Our long term goal is to use the knowledge we gain about plant-pathogen interactions to engineer plants for increased resistance to diseases and thereby lessen the need for synthetic chemical inputs.

PLPA 452.1 / PLPA 662.1 Molecular Plant-Microbe Interactions: Plant Responses to Pathogen Attack. 4-week module (1 credit. Taught in even-numbered years.