EAGER: Salicylic acid signaling in plant pathogen interactions

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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.