Extracellular recognition by plants of potential bacterial pathogens initiates rapid changes in plant responses that ultimately lead to restriction of bacterial growth and prevention of disease symptoms. Achievement of the desired outcome of host resistance, however, is a finely balanced process. If the initial host response is not sufficiently rapid or robust, the pathogen overwhelms the host before effective resistance can be achieved. If the response is too strong or lasts for too long, the stress can result in severe fitness penalties (e.g. dwarfing and/or loss of yield) or even cell death. At present, relatively little about is understood about how the initial responses are correctly regulated and integrated to promote resistance. MAP Kinase Phosphatase 1 (MKP1) has been identified as a negative regulator of both the initial phases of host responses and of resistance against pathogenic bacteria. However, unlike most plants with enhanced resistance, the mkp1 mutation prevents bacterial pathogen growth without apparent detrimental effects on the plant's fitness. Therefore, understanding the role and regulation of MKP1 in plant innate immunity will illuminate possible strategies for enhancing resistance against bacteria in crop plants without the fitness penalties normally associated with constitutively enhanced resistance. Genetic, biochemical, and molecular approaches will be used to begin to define the basis for the enhanced resistance in the mkp1 mutant as well as to understand how MKP1 is normally regulated during pathogen infection.
The project will provide advanced training for both a postdoctoral researcher and graduate student as well as for an undergraduate EXPRESS (Exposure to Research for Science Students) student already working in the laboratory, thus providing support for students from a minority group normally underrepresented in the sciences.
