Arabidopsis basal innate immunity to bacterial infection

这项研究的长期目标是阐明植物的明显相互交织的分子基础 对植物病原体的易感性和植物对人类病原体的基础免疫力。在自然界中，植物 对大多数微生物免疫，包括大多数人类病原体;然而，植物 易受已进化出特定毒力策略的植物病原细菌亚类的影响。之一 最重要的细菌毒力策略是III型分泌系统，该系统注入多种多样的 进入宿主细胞以促进发病。知之甚少的分子 这些效应蛋白调节植物细胞功能的机制。最近的研究表明， 令人兴奋的线索：一些效应蛋白参与抑制各种形式的植物免疫。在 特别是，两种假单胞菌效应子AvrPto和HopPtoM抑制了小鼠的基础先天免疫， 拟南芥。初步结果表明，AvrPto可能靶向极化的细胞外运输途径 由G蛋白的RabE家族介导。HopPtoM促进几种宿主蛋白的消失 （AtMIN）。阐明AvrPto和HopPtoM抑制基础免疫的分子机制 在拟南芥中，我们将（1）描述拟南芥中RabE介导的囊泡运输途径 免疫，（2）确定AvrPto抑制RabE功能的机制，（3）表征 （4）确定AtMIN蛋白在HopPtoM特异性毒力中的作用。 将采用分子遗传学、细胞生物学、转基因和病理学方法的综合方法， 为实现这些目标而采取的措施。这项研究不仅有助于基本的 细菌病原体如何在高等真核生物中引起疾病的知识，也增加了我们的 了解植物对人类病原体的免疫力的实际上未探索的分子基础。食品 由人类病原体污染引起的中毒是一个主要的公共卫生问题。

The long-term goal of this research is to elucidate the apparently intertwined molecular bases of plant susceptibility to plant pathogens and plant basal immunity to human pathogens. In nature, plants are immune to most microbes, including the majority of human pathogens; however, plants are extremely susceptible to a subset of phytopathogenic bacteria that have evolved specific virulence strategies. One of the most important bacterial virulence strategies is the type III secretion system, which injects a diverse array of effector proteins into the host cell to promote pathogenesis. Little is known about the molecular mechanisms by which these effector proteins modulate plant cellular functions. Recent studies have given exciting clues: some effector proteins are involved in suppressing various forms of plant immunity. In particular, two Pseudomonas syringae effectors, AvrPto and HopPtoM, suppress basal innate immunity in Arabidopsis. Preliminary results show that AvrPto may target a polarized extracellular trafficking pathway mediated by the RabE family of G proteins. HopPtoM promotes the disappearance of several host proteins (AtMINs). To elucidate the molecular mechanisms by which AvrPto and HopPtoM suppress basal immunity in Arabidopsis, we will (1) characterize the RabE-mediated vesicle trafficking pathway in Arabidopsis immunity, (2) determine the mechanism by which AvrPto inhibits RabE function, (3) characterize the virulence activity of HopPtoM, and (4) determine the role of AtMIN proteins in HopPtoM-specific virulence. An integrated approach using molecular genetic, cell biological, transgenic, and pathological methods will be taken to accomplish these aims. The proposed research will not only contribute to the fundamental knowledge of how bacterial pathogens cause disease in higher eukaryotes, but also increase our understanding of the virtually unexplored molecular basis of plant immunity to human pathogens. Food poisoning caused by human pathogen contamination is a major public health concern.