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

植物免疫调节因子的自然多样性和突变分析，合理设计作为诱饵的免疫蛋白

• 批准号: 1557661
• 负责人: Jennifer Lewis
• 金额: $ 54.97万
• 依托单位: University of California-Berkeley
• 依托单位国家: 美国
• 项目类别: Standard Grant
• 财政年份: 2016
• 资助国家: 美国
• 起止时间: 2016-05-15 至 2022-04-30
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=1557661&HistoricalAwards=false
• 关键词: Natural; Diversity; Mutant; Analysis; Regulators

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.

植物病原菌在世界范围内造成巨大的农作物损失，并迅速进化以压倒现有的寄主免疫力。许多病原体将效应蛋白运送到宿主体内，以促进病原体的毒力。随着进化时间的推移，植物可以进化来识别病原体的特定效应蛋白。国际和平研究所的研究小组发现了一种植物蛋白(“诱饵”)，它可以作为病原体效应蛋白的“捕鼠器”，并使植物能够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并保护作物免受感染。该项目包括向当地一所服务于不同学生群体的两年制大学提供大量服务，其中包括代表不足的群体(37%的西班牙裔、24%的非裔美国人、19%的亚裔、1%的夏威夷裔)和贫困学生(68%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。剖析寄主免疫的分子决定因素将提供一个严格的工具包，以对抗植物病原体带来的重大问题。HopZ1a是丁香假单胞菌III型分泌的效应蛋白，当HopZ1a乙酰化ZED1伪激酶时，通过富含亮氨酸重复序列的受体蛋白ZAR1间接识别。ZED1似乎是一个诱饵，它进化成了诱骗T3SE识别的诱饵，因为它不是一个功能激酶，在基础免疫中没有作用。这项工作将检查ZAR1和ZED1自然和突变的多样性，以便为合理设计病原体诱饵制定限制条件。PI将与当地一所两年制大学合作，该学院主要服务于贫困学生和代表不足的群体，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，该模块将在学院教授。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从事和擅长多学科的科学研究，为研究生和博士后提供外展机会，并在重大科学和农业问题上取得进展。