Arabidopsis basal innate immunity to bacterial infection

这项研究的长期目标是阐明植物表面上相互交织的分子基础。 植物对病原体的敏感性和植物对人类病原体的基础免疫。在自然界，植物是 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菌的子集影响。其中之一 最重要的细菌毒力策略是III型分泌系统，它注入了不同的阵列 效应蛋白进入宿主细胞促进发病。人们对这种分子知之甚少 这些效应蛋白调节植物细胞功能的机制。最近的研究给出了 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……里面 特别是，两种丁香假单胞菌效应物，AvrPto和HopPtoM，抑制了基础先天免疫 拟南芥。初步结果表明，AvrPto可能以极化的细胞外转运途径为靶点 由拉贝G蛋白家族介导。HopPtoM促进几种宿主蛋白的消失 (AtMins)。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RABE介导的小泡运输途径 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。 使用分子遗传学、细胞生物学、转基因和病理学方法的综合方法将是 来实现这些目标。拟议中的研究不仅将有助于 关于细菌病原体如何在高等真核生物中致病的知识，也增加了我们的 了解植物对人类病原体免疫的几乎未知的分子基础。食物 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.