Bacterial diseases of plants cause significant losses in overall yield and marketability of many economically-important US crops. Although plants possess an immune system that can provide effective resistance against infection, bacteria have evolved sophisticated counter-measures that can effectively suppress these host defenses. As a result, a major determinant of infection outcome is how rapidly both bacteria and host plant can deploy their respective virulence and defense strategies. This project will investigate the molecular basis for chemical signaling events that occur between plants and bacteria at the onset of infection, with a focus on how pathogenic bacteria perceive plant-derived metabolite signals to begin their infection process. Non-specific antimicrobials such as copper sprays and broad-spectrum antibiotics are frequently used to control bacterial diseases in crops. This project will provide a deeper understanding of host perception mechanisms in bacteria that could lead to development of specific chemical inhibitors of this process, thereby providing alternative methods to control disease and potentially improve crop fitness. The project will also provide opportunities for undergraduate students at smaller resource-limited colleges to gain research experience through internships in the investigator's laboratory. Furthermore, a workshop on proteomics methodology will be developed and delivered by the investigator as part of a two-week summer STEM camp for high school students.
Genes encoding the virulence-promoting type III secretion system (T3SS) of the plant pathogen Pseudomonas syringae must be expressed at early stages of infection for this bacterium to be fully virulent. In previous work, the investigator identified plant-derived metabolites that induce the expression of T3SS-encoding genes in P. syringae. Although the bioactive plant metabolites are potent enhancers of virulence, how they are perceived by P. syringae to initiate expression of its T3SS is not known. A primary objective of this project is to elucidate the genetic basis for host recognition by P. syringae with a goal of identifying potential receptor proteins that are directly involved in perceiving host metabolite signals. A second objective is elucidate why a P. syringae gacA- mutant that hyper-expresses its T3SS is less virulent, with the goal of understanding how P. syringae coordinates the deployment of virulence factors to maximize pathogenicity. Lastly, exogenous application of T3SS-inducing metabolites during P. syringae infection of Arabidopsis suppresses enhanced resistance mediated by plant pathogen recognition receptors (PRRs), suggesting a mechanism of PRR-dependent resistance may be the removal of these metabolite signals or interference with their perception. This project will investigate if extracellular levels of the bioactive metabolites change following PRR activation in Arabidopsis plants. Insights into this possible mechanism of plant defense may lead to the development of engineered crop plants that deploy PRR-mediated defenses in a more effective and targeted manner.
