Defining the molecular plant-pathogen interface

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As the global population continues to rise, bringing with it an increased demand for food, it will be crucial to engineer pest-resistant crops or develop robust, environmentally friendly disease control strategies to answer this demand effectively. The development of effective and durable disease control strategies requires extensive knowledge of host immune systems as well pathogen virulence strategies. Importantly, these two systems are interdependent and have shaped each other's evolutionary trajectory in a perpetual host-pathogen "arms race". At the molecular level, the interface between pathogen virulence factors and host proteins is where this arms race is played out. As such, this interface represents a unique opportunity to investigate both the mechanisms of pathogen virulence as well as host resistance, and also to provide insights into the evolutionary pressures shaping these interactions. The bacterial phytopathogen Pseudomonas syringae can infect and cause disease on hundreds of plant species. Like many Gram-negative bacterial pathogens, the ability of P. syringae to cause disease is dependent on the repertoire of effector proteins delivered into host cells by a molecular syringe called the type III secretion system. Type III-secreted effector proteins of P. syringae target several plant cellular systems in order to dampen host immunity and promote infection. However, the molecular details of these interactions are limited and represent a major challenge of current studies in plant-microbe interactions. The goal of this proposal is to characterize the molecular interface between P. syringae Type III-secreted effector proteins and their host targets in order to understand how pathogens cause disease and how plants have evolved to resist the infection process.