Manipulation of Plant Signaling by Bacterial Effector Proteins

植物是否对病原体具有抗性取决于两种生物体的基因组成。病原体产生效应蛋白，为病原体的利益操纵植物。植物产生抗性或r蛋白，识别效应物并诱导防御，限制病原体的生长。最近克隆的基因编码效应和r蛋白使其相互作用的机制研究的分子和生化方法。本文主要研究拟南芥及其病原菌丁香假单胞菌。这些模式生物提供了丰富的工具，有助于回答基本的生物学问题，例如：病原体如何通过使用效应物来操纵它们，从而更成功地寄生在植物上？r蛋白如何使植物通过识别效应物和诱导防御反应来限制病原体生长？具体来说，本研究的重点是多种细菌效应物靶向的植物蛋白（RIN4）。一个主要的焦点是确定细菌效应物如何靶向RIN4增强细菌的毒力（或致病性）。RIN4还调节对这些效应物作出反应的r蛋白的功能。第二个主要焦点是确定由效应蛋白诱导的对RIN4的操作如何引起r蛋白的活性。这个项目很重要，因为目前对植物中致病效应物与其靶点之间的相互作用知之甚少。对这些相互作用的基本理解将促进对病原体如何引起植物疾病以及植物如何抵抗病原体的理解。这些信息最终将有助于通过传统育种努力或引入转基因来合理设计优质作物。在分子水平上理解这些过程也将有助于合理设计新的化学品来控制作物的疾病。这项研究的意义超出了病原体与植物的相互作用。病原体编码的效应物类似地操纵动物宿主中的靶标，对植物中效应物作用的理解的进展将导致对所有生物中这一过程的更好的基本理解。学生将被训练进行这一领域的研究。

Whether plants are resistant to pathogens depends on the genetic make-up of both organisms. Pathogens produce effector proteins that manipulate the plant for the pathogen's benefit. Plants produce resistance or R-proteins that recognize effectors and induce defenses that restrict pathogen growth. Recent cloning of genes encoding effectors and R-proteins enables mechanistic study of their interactions by molecular and biochemical methods. This research focuses on Arabidopsis thaliana plants and their bacterial pathogen Pseudomonas syringae. These model organisms offer a wealth of tools useful in answering fundamental biological questions, such as: How do pathogens more successfully parasitize plants by using effectors to manipulate them? How do R-proteins enable plants to restrict pathogen growth by recognizing effectors and inducing defense responses? Specifically, this research focuses on a protein of the plant (RIN4) that is targeted by multiple bacterial effectors. One major focus is to determine how targeting of RIN4 by bacterial effectors enhances the virulence (or pathogenicity) of the bacteria. RIN4 also regulates the function of R-proteins that respond to those effectors. A second major focus is to determine how manipulation of RIN4, induced by effector proteins, elicits the activity of R-proteins.This project is important because little is currently known about the interactions between pathogenic effectors and their targets in plants. Fundamental understanding of these interactions will advance understanding of how pathogens cause disease in plants and of how plants resist pathogens. This information will ultimately contribute to the rational design of superior crops by classical breeding efforts or by introduction of transgenes. Understanding these processes at the molecular level will also enable rational design of new chemicals to manage disease in crops. The significance of this research extends beyond the interaction of pathogens with plants. Pathogen encoded effectors similarly manipulate targets in animal hosts, and advances in understanding of effector action in plants will lead to a better fundamental understanding this process in all organisms. Students will be trained to conduct research in this field.