Arabidopsis basal innate immunity to bacterial infection

拟南芥对细菌感染的基础先天免疫

• 批准号: 7321663
• 负责人: SHENG YANG HE
• 金额: $ 34.74万
• 依托单位: MICHIGAN STATE UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-12-15 至 2010-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7321663
• 关键词: ATP phosphohydrolase; Arabidopsis; Arabidopsis Proteins; Bacteria; Bacterial Infections; Binding; Biological; Cell physiology; Cells; Disease; Endopeptidases; Eukaryota; Eukaryotic Cell; Family; Flagellin; Food Poisoning; GTP-Binding Proteins; GTPase-Activating Proteins; Goals; Human; Immune; Immune response; Immunity; Knowledge; Mediating; Methods; Microbe; Modeling; Molecular; Molecular Genetics; Monomeric GTP-Binding Proteins; Natural Immunity; Nature; Pathogenesis; Pathway interactions; Peptide Hydrolases; Plants; Predisposition; Proteins; Pseudomonas aeruginosa; Pseudomonas syringae; Public Health; Range; Research; Role; Salmonella; System; Testing; Transgenic Organisms; Type III Secretion System Pathway; Vesicle; Virulence; base; extracellular; inhibitor/antagonist; microbial; mutant; novel; pathogen; pathogenic bacteria; response; trafficking

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.

这项研究的长期目标是阐明植物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，植物是 对大多数微生物（包括大多数人类病原体）具有免疫力；然而，植物极其 对已经进化出特定毒力策略的植物病原细菌的子集敏感。之一 最重要的细菌毒力策略是 III 型分泌系统，它注入多种阵列 效应蛋白进入宿主细胞以促进发病机制。人们对分子知之甚少 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 特别是，两种丁香假单胞菌效应子 AvrPto 和 HopPtoM 抑制基础先天免疫 拟南芥。初步结果表明 AvrPto 可能针对极化的细胞外运输途径 由 G 蛋白 RabE 家族介导。 HopPtoM 促进多种宿主蛋白​​的消失 （AtMINs）。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 HopPtoM 的毒力活性，(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 为实现这些目标而采取的措施。拟议的研究不仅有助于基础研究 了解细菌病原体如何在高等真核生物中引起疾病​​，同时也增加了我们的知识 了解植物对人类病原体免疫的几乎未经探索的分子基础。食物 人类病原体污染引起的中毒是一个重大的公共卫生问题。