Natural Diversity and Mutant Analysis of Regulators of Plant Immunity for Rational Design of Immunity Proteins as Decoys

植物病原体在世界范围内造成巨大的作物损失，并迅速进化以压倒现有的宿主免疫。许多病原体将效应蛋白传递到宿主体内，以增强病原体的毒力。随着进化时间的推移，植物可以进化到识别来自病原体的特定效应蛋白。PI的研究小组已经确定了一种植物蛋白（一种“诱饵”），它可以作为病原体效应蛋白的“捕鼠器”，并使植物产生强烈的免疫反应。这项工作将确定在宿主中识别病原体所需的遗传参数，以帮助设计更好的诱饵和保护作物免受感染。该项目包括向当地一所两年制大学提供大量服务，该学院为多元化的学生群体提供服务，包括代表性不足的群体（37%的西班牙裔，24%的非洲裔美国人，19%的亚裔，1%的夏威夷人）和贫困学生（68%的人获得经济援助），以便让学生接触尖端研究和更广泛的教育机会。解剖宿主免疫的分子决定因素将为对抗植物病原体带来的重大问题提供一个严格的工具包。HopZ1a是丁香假单胞菌III型分泌的效应蛋白，当HopZ1a乙酰化ZED1假激酶时，通过ZAR1间接识别。ZAR1是一种富含亮氨酸重复序列的核苷酸结合位点受体蛋白。ZED1似乎是一个诱饵，它已经进化到诱骗T3SE进入识别，因为它不是一个功能性激酶，在基础免疫中没有作用。这项工作将检查ZAR1和ZED1的自然和突变多样性，以便为合理设计病原体诱饵制定约束。PI将与当地一所两年制大学合作，该大学主要为贫困学生和弱势群体提供服务，并将在每年夏天接待几名学生学习新的科学技术。该实验室将设计一个关于植物免疫的模块，并将在学院授课。这将为学生和博士后提供教学机会，并增加未被充分代表的群体对科学的参与。这些努力将鼓励代表性不足的学生追求并在多学科科学研究中脱颖而出，为研究生和博士后提供拓展机会，并在重大科学和农业问题上取得进展。

Plant pathogens cause tremendous crop losses worldwide and evolve quickly to overwhelm existing host immunity. Many pathogens deliver effector proteins into their hosts to promote virulence of the pathogen. Over evolutionary time, the plant can evolve to recognize specific effector proteins from the pathogen. The PI's research group has identified a plant protein (a "decoy") that acts as a "mousetrap" for a pathogen effector protein, and enables the plant to mount a strong immune response. This work will determine the genetic parameters necessary for pathogen recognition in the host, in order to help design better decoys and protect crops from infection. This project includes substantial outreach to a local two-year college that serves a diverse student body, including underrepresented groups (37% Hispanic, 24% African American, 19% Asian, 1% Hawaiian) and underprivileged students (68% receive financial aid), in order to expose students to cutting-edge research and broader educational opportunities. Dissection of the molecular determinants underlying host immunity will provide a rigorous toolkit to combat the significant problem posed by plant pathogens. HopZ1a, a Pseudomonas syringae type III secreted effector protein, is recognized indirectly through ZAR1, a nucleotide-binding site leucine-rich repeat containing receptor protein, when HopZ1a acetylates the ZED1 pseudokinase. ZED1 appears to be a decoy that has evolved to trap the T3SE into recognition, as it is not a functional kinase and does not have a role in basal immunity. This work will examine ZAR1 and ZED1 natural and mutant diversity in order to develop constraints for rational design of a pathogen decoy. The PI will collaborate with a local two-year college that primarily serves underprivileged students and underrepresented groups, and will host several students each summer to learn new scientific techniques. The lab will design a module on plant immunity that will be taught in the college. This will provide teaching opportunities for students and post-docs, and increase the participation of underrepresented groups in science. Together these efforts will encourage underrepresented students to pursue and excel at multi-disciplinary scientific research, provide outreach opportunities for graduate students and post-docs, and make progress on significant scientific and agricultural problems.