MKP1 regulates plant metabolite signals that induce bacterial virulence: How and where are these signals controlled?

许多植物通常会受到细菌病原体的感染，从而导致粮食产量下降甚至死亡。然而，研究人员最近发现了一种突变植物，这种植物具有增强对细菌病原体抗性的新机制，从而防止细菌感染。在这个项目中，研究人员将通过研究控制这种抗性的位置和机制来确定突变体如何独特地阻止病原体。研究人员还将检查突变体是否增强了对其他类型病原体（例如真菌病原体）的抗性，或者突变是否会导致对一种病原体的抗性增强，而对另一种病原体的敏感性增加。该项目的目标是确定是否有一种新的遗传方法可以提高作物对病原体的存活率，而不会产生任何意外的惩罚。大多数病原菌表达第三类分泌系统（T3 SS），以抑制植物的免疫反应，从而使病原体获得复制所需的营养。研究人员最近发现了一种拟南芥突变体（mkp 1），它产生的诱导细菌中T3 SS的化学信号较少，从而导致植物的抗性增强。将这一发现转化为田间抗性的提高需要更好地理解其基本原理。MKP 1是否调节控制代谢物穿过质膜（PM）的转运蛋白水平以限制化学信号（通过定量质膜蛋白质组学解决）？MKP 1是否调节这些代谢物的细胞产生（通过定量代谢组学解决）？叶片中的所有细胞类型是否对代谢产物的产生以及因此产生的抗性（通过细胞/组织特异性互补来解决）做出了同等的贡献？最后，关键是要测试病原体的信息谱，以确定mkp 1的耐药性是否延伸到其他类型的病原体，或者更重要的是，mkp 1的变化是否可能产生负面影响，使其更容易受到无关病原体的影响。更好地理解这种明显新颖的抗性机制可能为提高田间可持续抗性提供重要基础。研究人员将扩大他们为本科生开发的植物生物学公共政策研讨会，让学生了解地方，州和国家层面的政策制定者如何影响大学的研究。学生将学习通过提供最有用的信息来传达基础研究的重要性。

Many plants normally become infected by bacterial pathogens that then cause reduced food yields or even death. However, the investigators recently discovered a mutant plant with a novel mechanism for enhanced resistance against bacterial pathogens whereby the plant prevents the bacteria from becoming infectious. In this project, the investigators will determine how the mutant uniquely stops the pathogen by studying both the location of and the mechanism(s) controlling this resistance. The investigators will also examine if the mutant has enhanced resistance against other types of pathogens (e.g. fungal pathogens) or if the mutation causes a trade-off of enhanced resistance against one type of pathogen at the expense of increased susceptibility to another. The goal of this project is to determine if there is a novel, genetic means of improving crop survival against pathogens without any unintended penalties.Most pathogenic bacteria express a type three secretion system (T3SS) to suppress the plant's immune responses, thus allowing the pathogen to acquire nutrients needed to replicate. The investigators recently identified an Arabidopsis mutant (mkp1) that produces less of the chemical signals that induce the T3SS in bacteria, thus resulting in a plant with enhanced resistance. Translating this discovery into improved resistance in the field requires a better understanding of the underlying principles. Does MKP1 regulate levels of transporters controlling movement of metabolites across the plasma membrane (PM) to restrict the chemical signals (addressed by quantitative plasma membrane proteomics)? Does MKP1 regulate the cellular production of these metabolites (addressed by quantitative metabolomics)? Do all cell types in the leaf contribute equally to the production of the metabolites and, therefore, resistance (addressed by cell/tissue-specific complementation? Finally, it is critical to test an informative spectrum of pathogens to determine if resistance in mkp1 extends to other types of pathogens or, perhaps more importantly, if the changes in mkp1 may have negative consequences making it more susceptible to unrelated pathogens. A better understanding of this apparently novel mechanism of resistance may provide an important basis for improving sustainable resistance in the field. The investigators will expand a Plant Biology & Public Policy Workshop they developed for undergraduates where students learn how policy makers at the local, state, and national level affect research at universities. Students will learn to communicate the importance of basic research by providing the most useful information.