The overall goal of this project is to develop an integrated program of research and education that advances knowledge of how bacterial pathogens infect plants, and introduces undergraduates and under-served high school students to the excitement of discovery in STEM. Bacterial diseases of plants cause significant losses in overall yield and marketability of many important US crops. Although plants have 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, an important determinant of infection outcomes is how rapidly both bacteria and host plant can deploy their respective virulence and defense strategies. This project will investigate chemical signaling events that occur between plants and bacteria, with a focus on how pathogenic bacteria perceive plant-derived metabolites to start an infection, as well as how plants may interfere with this perception process. Bacterial diseases in crops are frequently controlled by non-specific antimicrobials such as copper sprays. Knowledge gained from this project could lead to the development of novel chemical inhibitors of bacterial diseases, as well as engineered crops that are more disease resistant. Research objectives of this project will be integrated into three main educational activities: 1) on-campus summer STEM camps for students from under-served rural and urban high schools in Oregon and Washington, 2) training of students in a functional genomics course and 3) summer-long laboratory research internships for high school students.
The plant pathogen Pseudomonas syringae must rapidly deploy its type III secretion system (T3SS) at early stages of infection to be virulent. Specific plant-derived organic acids and amino acids, together with simple sugars, induce T3SS-encoding genes in P. syringae, yet how these signals are perceived is poorly understood. In previous work the investigator identified a transcription factor SetA that is required for maximal sugar-induced expression of T3SS genes in P. syringae. The project?s first objective is to determine how SetA regulates expression of T3SS master regulator hrpL and to identify the intracellular metabolite signal(s) that may regulate SetA activity. The investigator also identified a two-component system, AauS-AauR, that directly links detection of host-derived amino acid signals to regulation of T3SS-encoding genes. A second objective is to determine how host signals activate AauS and how the downstream response regulator AauR regulates T3SS-encoding genes. Proposed methods include biochemical approaches to assess protein-metabolite, protein-DNA and protein-protein interactions that regulate the functions of SetA and AauS-AauR. Using metabolomics, the investigator also discovered that specific T3SS-inducing metabolites decrease in abundance in leaves during a host defense response. The project?s third objective is to determine the molecular mechanism(s) that regulate the abundance of these metabolites, and how these host signals are perceived by P. syringae through AauS/AauR- and SetA-independent mechanisms.
This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.
