EAGER: Salicylic acid signaling in plant pathogen interactions

植物在其一生中面临着多种非生物和生物胁迫。主要威胁包括真菌、卵菌、病毒、细菌和线虫病原体。据估计，这些植物病原体引起的疾病每年使植物产量减少10-20%。经过数百万年的分子相互作用和寄主植物及其病原体的共同进化，植物发展出了一种复杂的免疫系统，可以感知即将发生的感染并组织适当的防御反应。在这个过程中，水杨酸（SA）激素是一个关键和必不可少的参与者。虽然受到研究界的相当重视，但其在免疫中的作用的基本方面仍然未知。该项目旨在解决这种主要免疫调节剂实现其作用的基本新机制。这可能为培育抗病作物提供新的策略。作为植物防御的主要调控因子，NPR1蛋白是sa介导的系统性获得性抗性（SAR）和基础防御所必需的。在没有病原体或SA处理的情况下，大多数NPR1以低聚物的形式存在于细胞质中。经过病原体攻击或SA处理后，NPR1低聚物被还原为单体进入细胞核，作为转录辅激活因子，结合TGA转录因子激活植物防御基因的表达。最近的研究表明，NPR1及其类似物NPR3和NPR4以不同的亲和力与SA结合，并作为SA受体发挥作用。此外，PI还鉴定出了NPR1单体形成、植物防御基因表达和SAR所需的核激酶HEN3。值得注意的是，在酵母双杂交实验中，SA促进了NPR1和TGA1/4转录因子之间的相互作用，从而支持了SA和NPR1通过增加NPR1和TGA1/4之间的蛋白-蛋白相互作用来激活植物防御的假设。该项目旨在解决这一关键免疫信号中枢功能的分子机制。有待探索的机制包括HEN3激酶在调控NPR1功能中的作用，以及SA对NPR1/3/4与TGA1/4相互作用的影响。该项目的广泛影响包括一名博士后、一名研究生和四名本科生的参与，其中两名来自科学领域代表性不足的群体。

During their lifetime plants face many kinds of abiotic and biotic stresses. Major threats include fungal, oomycete, viral, bacterial and nematode pathogens. It is estimated that diseases caused by these plant pathogens reduce plant yield by 10-20% every year. Over millions of years of molecular interactions and co-evolution of host plants and their pathogens, plants developed a sophisticated immune system that senses an impending infection and organizes appropriate defense responses. A key and essential player in this process is the hormone salicylic acid (SA). Although receiving considerable attention from the research community, essential aspects of its role in immunity remain unknown. This project seeks to resolve fundamental new mechanisms through which this major immune regulator achieves its effects. These may provide new strategies for developing disease resistant crop plants. As a master regulator of plant defense, the protein NPR1 is required for SA-mediated systemic acquired resistance (SAR) and basal defense. In the absence of pathogens or SA treatment, most NPR1 exists in the cytosol as oligomers. After pathogen challenge or SA treatment, NPR1 oligomers are reduced to monomers which enter the nucleus where they function as transcriptional coactivators, binding TGA transcription factors to activate the expression of plant defense genes. Recent publications demonstrated that NPR1 and its paralogs NPR3 and NPR4 bind SA with different affinities and function as SA receptors. In addition, the PI has identified HEN3, a nuclear kinase which is required for NPR1 monomer formation, plant defense gene expression and SAR. Significantly, SA promotes interactions between NPR1 and TGA1/4 transcription factors in a yeast two-hybrid assay, thus supporting the hypothesis that SA and NPR1 activate plant defense through increased protein-protein interactions between NPR1 and TGA1/4. This project seeks to resolve molecular mechanisms that underlie and regulate the function of this key immune signaling hub. Mechanisms to be explored include the role of the HEN3 kinase in regulating NPR1 function, and the effect of SA on interactions between NPR1/3/4 and TGA1/4. The broader impacts of the project include the participation of a postdoc, a graduate student and four undergraduates, including two from groups underrepresented in the sciences.