Role in Pathogenesis of Pseudomonas Syringae Proteins Targeted to the Plant Apoplast by the Type III Secretion System

III 型分泌系统靶向植物质外体的丁香假单胞菌蛋白在发病机制中的作用

• 批准号: 0544066
• 负责人: Alan Collmer
• 金额: --
• 依托单位: Cornell Univ - State: AWDS MADE PRIOR MAY 2010
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-03-01 至 2010-02-28
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0544066&HistoricalAwards=false
• 关键词: Role; Pathogenesis; Pseudomonas; Syringae; Proteins

Pseudomonas syringae pv. tomato DC3000 causes bacterial speck disease on tomato and Arabidopsis. DC3000 pathogenesis is dependent on the type III secretion system (TTSS), which translocates many effector proteins into plant cells. An important function of some effectors, such as AvrPto, is suppression of basal resistance (innate immunity) in plants. P. syringae also secretes several proteins through the TTSS that appear to be targeted to the plant apoplast rather than the cytoplasm. These "apoplast Hops" (Hrp outer proteins) include two proteins with a lytic transglycosylase domain: HopP1 and CEL (conserved effector locus) ORF1. The latter is encoded adjacent to the hrp/hrc genes encoding the TTSS. A P. syringae hrp/hrc cluster, cloned in P. fluorescens, enables this nonpathogen to translocate AvrPto into plant cells and to suppress basal resistance. Remarkably, P. fluorescens expressing the TTSS and either HopP1 or CEL ORF1 suppresses basal resistance in the absence of any effector. The specific objectives of this project are to: (i) identify all P. syringae tomato DC3000 apoplast Hops and test their ability to either elicit or suppress the hypersensitive response and basal resistance; (ii) determine the basis for the innate ability of the P. syringae TTSS to suppress basal resistance when expressed in a nonpathogen; (iii) construct mutations in P. s. tomato DC3000 and test the functions of apoplast Hops during interactions with host plants. This project should yield new insights into the TTSS and innate immunity, two factors important in bacterium-host interactions involving both plant and animal pathogens. The project has ongoing outreach activities with high schools and primarily undergraduate institutions.

丁香假单胞菌 pv.番茄 DC3000 会导致番茄和拟南芥细菌性斑点病。 DC3000 发病机制依赖于 III 型分泌系统 (TTSS)，该系统将许多效应蛋白易位到植物细胞中。一些效应子（例如 AvrPto）的一个重要功能是抑制植物的基础抗性（先天免疫）。丁香假单胞菌还通过 TTSS 分泌多种蛋白质，这些蛋白质似乎针对植物质外体而不是细胞质。这些“质外体啤酒花”（Hrp 外部蛋白）包括两种具有裂解性转糖基酶结构域的蛋白：HopP1 和 CEL（保守效应基因座）ORF1。后者的编码位置与编码 TTSS 的 hrp/hrc 基因相邻。荧光假单胞菌中克隆的丁香假单胞菌 hrp/hrc 簇使这种非病原体能够将 AvrPto 易位到植物细胞中并抑制基础抗性。值得注意的是，表达 TTSS 和 HopP1 或 CEL ORF1 的荧光假单胞菌在没有任何效应子的情况下抑制基础抗性。该项目的具体目标是： (i) 鉴定所有丁香番茄 DC3000 质外体啤酒花，并测试它们引发或抑制过敏反应和基础抗性的能力； (ii) 确定丁香假单胞菌 TTSS 在非病原体中表达时抑制基础抗性的先天能力的基础； (iii) 在 P. s 中构建突变。番茄 DC3000 并测试质外体啤酒花在与宿主植物相互作用过程中的功能。该项目应该对 TTSS 和先天免疫产生新的见解，这两个因素在涉及植物和动物病原体的细菌-宿主相互作用中很重要。该项目正在与高中和主要是本科院校开展外展活动。