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

植物对潜在细菌病原体的细胞外识别启动了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。如果宿主最初的反应不够迅速或不够强烈，病原体就会在宿主产生有效耐药性之前将其压倒。如果反应太强烈或持续时间太长，则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，关于如何正确调节和整合初始反应以促进耐药性的了解相对较少。MAP激酶磷酸酶1 （MKP1）已被确定为宿主反应初始阶段和对致病菌抗性的负调节因子。然而，与大多数具有增强抗性的植物不同，mkp1突变可以阻止细菌病原体的生长，而不会对植物的适应性产生明显的有害影响。因此，了解MKP1在植物先天免疫中的作用和调控，将阐明提高作物对细菌抗性的可能策略，而不会出现通常与组成性增强抗性相关的适应度损失。将使用遗传、生化和分子方法开始确定mkp1突变体增强抗性的基础，并了解mkp1在病原体感染期间如何正常调节。该项目将为一名博士后研究员和研究生以及一名已经在实验室工作的本科生提供高级培训，从而为来自通常在科学领域代表性不足的少数群体的学生提供支持。

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.