Defining the molecular plant-pathogen interface

定义分子植物-病原体界面

• 批准号: 327234-2011
• 负责人: Desveaux, Darrell
• 金额: $ 2.91万
• 依托单位: University of Toronto
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2015
• 资助国家: 加拿大
• 起止时间: 2015-01-01 至 2016-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=571958
• 关键词: Defining; molecular; plant; pathogen; interface

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.

随着全球人口持续增长，对粮食的需求也随之增加，设计抗虫作物或制定强有力的、环境友好的疾病控制策略来有效满足这一需求至关重要。制定有效且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，并在永恒的宿主-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上演的地方。因此，该界面提供了一个独特的机会来研究病原体毒力和宿主抵抗力的机制，并提供对塑造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数百种植物并引起疾病。与许多革兰氏阴性细菌病原体一样，丁香假单胞菌引起疾病的能力取决于通过称为 III 型分泌系统的分子注射器递送到宿主细胞中的效应蛋白的全部成分。丁香假单胞菌分泌的 III 型效应蛋白以多种植物细胞系统为目标，以抑制宿主免疫力并促进感染。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。该提案的目标是表征丁香假单胞菌 III 型分泌的效应蛋白与其宿主靶标之间的分子界面，以了解病原体如何引起疾病以及植物如何进化以抵抗感染过程。