Defining the molecular plant-pathogen interface

随着全球人口的持续增长，随之而来的是对粮食的需求增加，因此设计抗虫害作物或制定强有力的、环境友好型疾病控制战略以有效满足这一需求将是至关重要的。开发有效和持久的疾病控制策略需要对宿主免疫系统以及病原体毒力策略的广泛了解。重要的是，这两个系统是相互依存的，并在一场永久的宿主-病原体“军备竞赛”中塑造了彼此的进化轨迹。在分子水平上，病原体毒力因子和宿主蛋白之间的界面是这场军备竞赛的展开之处。因此，这种界面代表了一个独特的机会，既可以研究病原菌毒力和寄主抗性的机制，也可以提供对形成这些相互作用的进化压力的洞察。植物病原菌丁香假单胞菌可侵染数百种植物并引起病害。像许多革兰氏阴性细菌病原体一样，丁香假单胞菌的致病能力取决于一种名为III型分泌系统的分子注射器将效应蛋白输送到宿主细胞的能力。丁香疫霉分泌的III型效应蛋白以多种植物细胞系统为靶标，以抑制宿主免疫，促进感染。然而，这些相互作用的分子细节是有限的，并且是当前植物-微生物相互作用研究的主要挑战。该建议的目的是表征丁香疫霉III型分泌的效应蛋白与其宿主靶标之间的分子界面，以了解病原体是如何引起疾病的，以及植物是如何进化来抵抗感染的。

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.