Current Research and Scholarly Interests
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 my research has been to elucidate T3S effector function, identify host targets, and provide fundamental knowledge of how perturbation of host signaling pathways leads to bacterial pathogenesis. To do so, we study the T3S effectors in Xanthomonas campestris pathovar vesicatoria (Xcv), the causal agent of leaf spot disease.
Our research currently focuses on the characterization of three Xcv T3S effectors: XopN, XopD, and AvrBsT. We discovered that these effectors modulate three distinct nodes of defense signal transduction, supporting the paradigm that T3S effectors encode defense suppressors. In addition, our work challenges this paradigm by demonstrating that one effector suppresses disease symptom development, thus illuminating the importance of tolerance promoting factors in bacterial-plant interactions. A few of our important findings include:
1) a novel screen to identify new Xanthomonas T3S effector proteins translocated into plant cells during infection
2) demonstrating that the XopN effector suppresses basal defense and physically interacts with a new tomato receptor kinase associated with basal immunity
3) demonstrating that the XopD effector is a plant-specific SUMO protease that represses host transcription, promotes pathogen growth, and suppresses host defense responses at the late stages of tissue colonization
4) identifying new proteins that control phospholipid signaling and disease resistance responses following AvrBsT perturbation