Our primary interest is in understanding the genetic and biochemical basis of disease resistance in plants. Plants are able to specifically recognize pathogens and actively respond. We are investigating how this specific recognition is accomplished and how recognition is translated into a resistant response.
To address these questions we take a molecular genetic approach. We use the small mustard Arabidopsis thaliana as our standard host plant, and the bacterial pathogen Pseudomonas syringae as our standard pathogen. Recognition of specific P. syringae strains by Arabidopsis is mediated by specific disease resistance (R) genes of Arabidopsis. These R genes are thought to encode receptors that detect a signal produced directly or indirectly by bacterial proteins that are injected into the plant cell. The molecular mechanism of this detection step is poorly understood, however. Understanding this mechanism is a major goal in plant biology as it will likely lead to new approaches for engineering disease resistance in plants, as well as provide critical insights into how pathogens evolve to escape recognition and cause disease.
To uncover the molecular basis of pathogen recognition we have focused on identifying genes in both the plant and the pathogen that are required for the recognition event. This has been accomplished by screening for plant mutants that fail to respond to bacteria expressing specific effector proteins that are secreted into the plant cells. To date we have cloned two R genes (RPM1 and RPS5) and have identified four additional genes (PBS1, PBS2, PBS3, and EDR1) believed to mediate signal transduction events. RPM1 and RPS5 belong to a very large gene family in plants. Each member of this family mediates recognition of a specific pathogen molecule. All members of this R gene family contain a nucleotide binding site (e.g. ATP) and leucine rich repeats (LRRs). The LRRs are thought to mediate protein: protein interactions, and may possibly participate in binding pathogen molecules or the targets of pathogen molecules. Very recent data indicate that the PBS1 protein may be such a target, and that the RPS5 protein may be detecting a modification of PBS1 induced by the pathogen. We are now using a combination of biochemical and genetic approaches to further test this model. In addition, we have recently isolated a disease resistance gene from soybean that has the same specificity as RPM1. By comparing the soybean gene to the Arabidopsis gene, we expect to gain additional insights into how specificity is determined. These analyses may in turn allow us to develop "designer R genes" that have novel specificities for use in real world agriculture.
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