Molecular Basis of Arabidopsis Susceptibility to Pseudomonas Syringae Infection

在植物和病原微生物的共同进化中，大多数植物都发展出了复杂的防御机制来抵御大多数（但不是全部）潜在的病原微生物。 当植物未能建立防御反应，而病原体携带适当的正毒力因子时，就会发生疾病。 在过去的十年中，人们投入了大量的精力来研究植物如何抵御病原体。 紫丁香假单胞菌-丁香假单胞菌病理系统的使用在促进病原体识别和植物抗性反应的理解方面发挥了关键作用。 相比之下，很少有人知道植物如何无法保护自己，并最终屈服于有毒病原体的感染。本研究的目的是了解假单胞菌引起拟南芥感染的分子机制。 这项研究是基于最近的发现，即人类，动物和植物的大多数细菌病原体使用专门的蛋白质分泌系统（III型分泌系统）主动将毒力蛋白“注入”宿主细胞。影响该病原体分泌系统的突变通常消除病原体感染相应宿主的能力，表明“III型毒力蛋白”在调节宿主易感性中的重要作用。 然而，这些III型毒力蛋白影响宿主信号传导和代谢过程的分子机制，最终导致易感相互作用的建立，在任何系统中都不清楚。 在这项研究中，提出了两个具体目标。 第一个目标是将Pst DC 3000感染的影响与特定拟南芥应答基因的表达联系起来。 这一目标的成功实现将消除一个主要的障碍，在易感宿主-细菌相互作用的研究进展，即缺乏宿主细胞和分子标记。 该提案的第二个目标是深入了解特定的III型毒力蛋白VirPtoB如何调节宿主易感性。 重点将是如何VirPtoB，当转基因表达拟南芥叶细胞内，改变拟南芥基因的表达和响应病原体感染。 这项研究涉及使用基因组，转基因和致病的方法。 这项研究的成功完成将有助于我们理解那些植物细胞机制，必须改变植物变得对病原体敏感。 在本研究项目的过程中，将培养一名博士后和一名本科生。

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.