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My laboratory studies the biochemical mechanisms used by bacterial pathogens to alter plant physiology during infection. Extensive genetic and phenotypic data indicate that the bacterial type three secretion (T3S) system and its protein substrates (referred to as T3S effectors) are the major virulence determinants that promote pathogen colonization in plants. The paradigm for T3S effector function has been that these proteins collectively suppress host defense responses to promote colonization and disease progression. The biological function(s) of most T3S effectors, however, is extremely limited and biochemical support for this paradigm is lacking. Thus, the goal of our research has been to elucidate T3S effector function, identify host targets, and provide fundamental knowledge of how perturbation of of distinct nodes in host signaling pathways leads to bacterial pathogenesis. To do so, we study the T3S effectors in Xanthomonas euvesicatoria (Xcv), a Gram-negative, facultative parasite that causes leaf spot disease in tomato and pepper. Understanding how plant innate immunity is regulated and how pathogens manipulate plant hosts is is fundamental knowledge that is required for the development of novel strategies to prevent and/or eliminate plant disease in the field.Currently, my group is investigating: 1) how Xanthomonas employs a transcription repressor to rewire host transcription during infection to alter immune signaling and growth programs; 2) how Xanthomonas effectors target 14-3-3 phospho-binding proteins to alter immune complexes and signaling; 3) the impact of Xanthomonas-mediated acetylation of host proteins that are involved with lipid signaling and microtubule dynamics; 4) how Xanthomonas uses a "default to death and defense strategy" to promote plant pathogenesis; and 5) unique natural products made during pathogen infection in tomato by applying a untargeted metabolomics in conjunction with transcriptomics to accelerate the discovery of new antimicrobial compounds and their biosynthetic pathways.