Defining the molecular plant-pathogen interface

随着全球人口的持续增长，对粮食的需求也随之增加，设计抗虫害作物或制定强大的、环境友好的疾病控制战略来有效地满足这一需求将是至关重要的。有效和持久的疾病控制策略的发展需要广泛的宿主免疫系统知识以及病原体毒力策略。重要的是，这两个系统是相互依存的，并在永久的宿主-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质之间的界面是这场军备竞赛进行的地方。因此，这个界面代表了一个独特的机会来研究病原体毒力和宿主抗性的机制，也提供了对形成这些相互作用的进化压力的见解。细菌植物病原体丁香假单胞菌可以感染并引起数百种植物的疾病。像许多革兰氏阴性细菌病原体一样，丁香假单胞菌致病的能力依赖于被称为III型分泌系统的分子注射器输送到宿主细胞中的效应蛋白。丁香假单胞菌iii型分泌效应蛋白以多种植物细胞系统为靶点，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，并且代表了当前植物-微生物相互作用研究的主要挑战。本研究的目的是表征丁香假单胞菌iii型分泌效应蛋白与其宿主靶标之间的分子界面，以了解病原体如何引起疾病以及植物如何进化以抵抗感染过程。

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.