Role and Regulation of MAP Kinase Phosphatase 1 as a Negative Regulator of Plant Innate Immune Responses

MAP 激酶磷酸酶 1 作为植物先天免疫反应负调节剂的作用和调节

• 批准号: 1051286
• 负责人: Scott Peck
• 金额: $ 48万
• 依托单位: University of Missouri-Columbia
• 依托单位国家: 美国
• 项目类别: Continuing Grant
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-09-01 至 2015-08-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=1051286&HistoricalAwards=false
• 关键词: Role; Regulation; MAP; Kinase; Phosphatase

Extracellular recognition by plants of potential bacterial pathogens initiates rapid changes in plant responses that ultimately lead to restriction of bacterial growth and prevention of disease symptoms. Achievement of the desired outcome of host resistance, however, is a finely balanced process. If the initial host response is not sufficiently rapid or robust, the pathogen overwhelms the host before effective resistance can be achieved. If the response is too strong or lasts for too long, the stress can result in severe fitness penalties (e.g. dwarfing and/or loss of yield) or even cell death. At present, relatively little about is understood about how the initial responses are correctly regulated and integrated to promote resistance. MAP Kinase Phosphatase 1 (MKP1) has been identified as a negative regulator of both the initial phases of host responses and of resistance against pathogenic bacteria. However, unlike most plants with enhanced resistance, the mkp1 mutation prevents bacterial pathogen growth without apparent detrimental effects on the plant's fitness. Therefore, understanding the role and regulation of MKP1 in plant innate immunity will illuminate possible strategies for enhancing resistance against bacteria in crop plants without the fitness penalties normally associated with constitutively enhanced resistance. Genetic, biochemical, and molecular approaches will be used to begin to define the basis for the enhanced resistance in the mkp1 mutant as well as to understand how MKP1 is normally regulated during pathogen infection. The project will provide advanced training for both a postdoctoral researcher and graduate student as well as for an undergraduate EXPRESS (Exposure to Research for Science Students) student already working in the laboratory, thus providing support for students from a minority group normally underrepresented in the sciences.

植物对潜在细菌病原体的细胞外识别引发植物反应的快速变化，最终导致细菌生长的限制和疾病症状的预防。然而，实现宿主抗性的预期结果是一个精细平衡的过程。如果最初的宿主反应不够迅速或稳健，病原体就会在宿主获得有效抗性之前将其消灭。如果反应太强或持续时间太长，压力可能导致严重的适应性惩罚（例如矮化和/或产量损失）甚至细胞死亡。目前，关于初始反应如何被正确调节和整合以促进抗性的了解相对较少。MAP激酶磷酸酶1（MKP 1）已被鉴定为宿主反应和对病原菌抗性的初始阶段的负调节剂。然而，与大多数具有增强抗性的植物不同，mkp 1突变阻止了细菌病原体的生长，而对植物的适应性没有明显的不利影响。因此，了解MKP 1在植物先天免疫中的作用和调节将阐明增强作物对细菌的抗性而不存在通常与组成性增强抗性相关的适应性惩罚的可能策略。 遗传学、生物化学和分子生物学方法将用于开始确定mkp 1突变体增强抗性的基础，以及了解在病原体感染期间Mkp 1通常是如何调节的。该项目将为博士后研究人员和研究生以及已经在实验室工作的本科生EXPRESS（理科学生接触研究）学生提供高级培训，从而为来自科学领域通常代表性不足的少数群体的学生提供支持。