Lon-Mediated Regulation of Type III Protein Secretion in Pseudomonas Syringae

Lon 介导的丁香假单胞菌 III 型蛋白分泌调节

• 批准号: 0215417
• 负责人: Steven Hutcheson
• 金额: $ 33万
• 依托单位: University of Maryland, College Park
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-08-15 至 2006-07-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=0215417&HistoricalAwards=false
• 关键词: Lon; Mediated; Regulation; Type; III

The pathogenicity and host range of Pseudomonas syringae, a plant pathogenic bacterium, has been linked to the activities of a type III protein secretion system (TTSS) that essentially injects bacterial proteins into cells of its host. These injected proteins alter the host cells to assist the growth of the bacterium in susceptible plants, but in resistant plants these proteins serve as a signal to initiate cellular defense mechanisms associated with disease resistance. The assembly of the TTSS in P. syringae is induced during the interaction with host cells and is coordinated by a complex genetic regulatory system. Positive- and negative-acting regulatory factors that control assembly of the TTSS have been identified. This project will elucidate how these regulatory factors transduce signals produced during the interaction with the host to regulate and coordinate assembly of the TTSS. This research will determine how the activity of a specific regulatory protease is controlled during the disease process, define the role of another regulatory protein, HrpV, in coordinating the assembly of the TTSS, examine a possible gating mechanism controlling when proteins are released from the bacteria, and elucidate how the activities of key transcriptional factors are modulated. The proposed experiments will provide new insight into molecular mechanisms for controlling bacterial disease and disease resistance in plants, but since several bacterial pathogens of mammals use a very similar mechanism, this research may have application to managing bacterial diseases of mammalian hosts.

植物病原细菌假单胞菌的致病性和宿主范围与III型蛋白质分泌系统（TTSS）的活性有关，所述III型蛋白质分泌系统（TTSS）基本上将细菌蛋白质注入其宿主细胞中。 这些注入的蛋白质改变宿主细胞，以帮助细菌在易感植物中生长，但在抗性植物中，这些蛋白质作为启动与抗病性相关的细胞防御机制的信号。 在与宿主细胞的相互作用过程中，诱导了P.dingae中TTSS的组装，并通过复杂的遗传调控系统进行协调。已经确定了控制TTSS组装的正作用和负作用调节因子。 本项目将阐明这些调节因子如何通过与宿主相互作用产生的信号来调节和协调TTSS的组装。 这项研究将确定在疾病过程中如何控制特定调节蛋白酶的活性，定义另一种调节蛋白HrpV在协调TTSS组装中的作用，检查控制蛋白质何时从细菌释放的可能门控机制，并阐明关键转录因子的活性如何调节。 拟议的实验将为控制植物细菌性疾病和抗病性的分子机制提供新的见解，但由于哺乳动物的几种细菌病原体使用非常相似的机制，这项研究可能适用于管理哺乳动物宿主的细菌性疾病。