Molecular Basis of Arabidopsis Susceptibility to Pseudomonas Syringae Infection

在植物和微生物病原体的共同进化中，大多数植物已经发展出复杂的防御机制来抵御大多数(但不是所有)潜在的病原体。当植物不能产生防御反应，而病原菌携带适当的正毒力因子时，就会发生病害。在过去的十年里，人们在研究植物如何抵御病原体方面投入了大量的努力。拟南芥-丁香假单胞菌致病系统的利用，对促进对病原菌识别和植物抗性反应的理解起到了至关重要的作用。相比之下，人们对植物如何未能自卫并最终屈服于剧毒病原体的感染知之甚少。本研究的目的是了解丁香假单胞菌侵染拟南芥的分子机制。这项研究是基于最近的一项发现，即大多数人类、动物和植物的细菌病原体使用一种特殊的蛋白质分泌系统(III型分泌系统)来主动地将毒力蛋白注入宿主细胞。影响这一病原体分泌系统的突变通常会消除病原体感染相应宿主的能力，这表明“III型毒力蛋白”在调节宿主敏感性方面发挥了重要作用。然而，这些III型毒力蛋白影响寄主信号和代谢过程的分子机制，最终导致敏感相互作用的建立，在任何系统中都不清楚。在本研究中，提出了两个具体目标。第一个目标是将PST DC3000感染的影响与特定的拟南芥反应基因的表达联系起来。这一目标的成功实现将消除在研究敏感宿主-细菌相互作用方面取得进展的一个主要障碍，即缺乏宿主细胞和分子标记。这项建议的第二个目标是深入了解一种特定的III型毒力蛋白VirPtoB如何调节宿主的敏感性。重点是当VirPtoB在拟南芥叶片细胞内转基因表达时，如何改变拟南芥基因的表达和对病原体感染的反应。这项研究涉及到基因组、转基因和致病方法的使用。这项研究的成功完成将有助于我们了解植物细胞机制，这些机制必须改变，才能使植物对病原体敏感。一名博士后和一名本科生将在本研究项目的过程中接受培训。

In the co-evolution between plants and microbial pathogens, most plants have developed sophisticated defense mechanisms to ward off the majority of (but not all) potential pathogens. When a plant fails to mount a defense response and the pathogen carries appropriate positive virulence factors, disease occurs. In the past decade, significant efforts have been invested in studying how plants defend against pathogens. The use of the Arabidopsis-Pseudomonas syringae pathosystem played a critical role in advancing the understanding of pathogen recognition and plant resistance responses. In contrast, very little is known about how a plant fails to defend itself and ultimately succumbs to infection by virulent pathogens. The goal of this research is to understand the molecular mechanism by which Pseudomonas syringae causes infection in Arabidopsis thaliana. This research is based on the recent finding that the majority of bacterial pathogens of humans, animals, and plants use a specialized protein secretion system (the type III secretion system) to actively "inject" virulence proteins into the host cell. Mutations affecting this pathogen secretion system often eliminate the ability of pathogens to infect the respective hosts, suggesting an important role of "type III virulence proteins" in modulating host susceptibility. However, the molecular mechanisms by which these type III virulence proteins affect host signaling and metabolic processes, which ultimately lead to the establishment of the susceptible interaction, is not understood in any system. In this research, two specific objectives are proposed. The first objective is to link the effects of Pst DC3000 infection to expression of specific Arabidopsis response genes. Successful accomplishment of this objective will remove a major roadblock to progress in the study of susceptible host-bacteria interactions, namely the lack of host cellular and molecular markers. The second objective of this proposal is aimed at achieving a deep understanding of how a specific type III virulence protein, VirPtoB, modulates host susceptibility. Emphasis will be on how VirPtoB, when transgenically expressed inside Arabidopsis leaf cells, alters Arabidopsis gene expression and response to pathogen infection. This research involves the use of genomic, transgenic, and pathogenic methods. Successful completion of this study will contribute to our understanding of those plant cellular mechanisms that must be altered for a plant to become susceptible to pathogens. A postdoctoral student and an undergraduate student will be trained during the course of this research project.