Dissecting the molecular plant-pathogen interface using type III effector proteins

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。这些疾病控制策略的发展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。然而，这些相互作用的分子细节是有限的，这是当前宿主-微生物相互作用研究的主要挑战。*Desveaux实验室使用多学科方法，使用假单胞菌丁香科/拟南芥模型病理系统来研究宿主-微生物相互作用。特别是，我们对感染过程中注入宿主细胞的一系列蛋白质着迷，这些蛋白质对许多革兰氏阴性细菌的毒力至关重要，包括丁香假单胞菌。这些蛋白质使用进化上保守的分子注射器注射，称为III型分泌系统。在宿主细胞内，III型效应器以特定的真核蛋白为靶标，为感染创造有利的环境。然而，III型分泌的效应器也可以将病原体的存在暴露给寄主，因为植物已经进化出检测特定III型效应器的抗性蛋白，以诱导强大的防御反应，从而阻止感染过程。因此，III型效应器是了解植物免疫的分子机制以及微生物毒力策略的宝贵探针。我们使用两个不同的丁香疫霉III型效应器家族在分子和生化水平上表征植物-微生物界面，以了解病原体是如何导致疾病的，以及植物是如何进化来抵抗感染过程的。**

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 these 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. However, the molecular details of these interactions are limited and represent a major challenge of current studies in host-microbe interactions.***The Desveaux lab uses a multidisciplinary approach to study host-microbe interactions using the Pseudomonas syringae / Arabidopsis thaliana model pathosystem. In particular, we are fascinated by a suite of proteins injected into host cells during the infection process that are essential for the virulence of many Gram negative bacterial pathogens including P. syringae. These proteins are injected using an evolutionarily conserved molecular syringe termed the type III secretion system. Inside host cells, type III secreted effectors target specific eukaryotic proteins in order to create a favourable environment for infection. However, type III secreted effectors can also betray the presence of the pathogen to its host since plants have evolved resistance proteins that detect specific type III effectors to induce a robust defence response that thwarts the infection process. As such, type III effectors represent invaluable probes to understand the molecular mechanisms of plant immunity as well as microbial virulence strategies. We are using two distinct families of P. syringae type III effectors to characterize the plant-microbe interface at the molecular and biochemical level in order to understand how pathogens cause disease and how plants have evolved to resist the infection process. **