My laboratory studies the biochemical mechanisms used by bacterial pathogens to alter plant physiology during infection. The long-term goal of our work is thus to elucidate the biochemical activities of bacterial virulence factors secreted by the type III secretory (T3S) apparatus, identify their host targets, and provide fundamental knowledge of how perturbation of these distinct nodes in plant signal transduction pathways leads to bacterial pathogenesis. To do so, we study bacterial leaf spot disease in tomato caused by the Gram-negative, facultative parasite Xanthomonas euvesicatoria (referred to as Xcv).
Initially, we performed a novel genetic screen to identify Xcv T3S effector proteins translocated directly into host plant cells during infection. We biochemically characterized the function of three Xcv T3S effectors – XopN, XopD, and AvrBsT. We have discovered that these effectors target three distinct nodes in defense signal transduction. We have shown that: 1) XopN encodes a novel scaffolding-like protein that suppresses PAMP-triggered immunity and physically interacts with the tomato atypical tomato receptor kinase TARK1and the 14-3-3 protein TFT1. 2) XopD encodes a plant-specific SUMO protease that represses host transcription, promotes pathogen growth, and suppresses host defense responses at the late stages of tissue colonization. 3) AvrBsT encodes an acetyltransferase that targets a microtuble-associated protein and interferes with lipid signaling, resulting in the activation of effector-triggered immunity.
Ongoing work is aimed at elucidating how the identified host targets regulate plant immunity during pathogen attack, as well as the biochemical characterization of novel core effectors that are conserved in Xanthomoans species. Understanding how plant immunity is regulated and how bacterial pathogens manipulate their hosts is fundamental knowledge required for the prevention and elimination of plant disease.