PhD Candidate University of Florida Gainesville, Florida
Body of Abstract: The redox metabolite NAD and its phosphorylated form NAD(P) are present intracellularly at millimolar concentrations and readily leak into the apoplast during infection where they are perceived by adjacent tissue to induce immunity to bacterial pathogens. We have shown that NAD(P) application suppresses hypersensitive response (HR) during infectionwithout compromising immunity. Here, we identify components required for NAD(P)-induced HR suppression, to further understand NAD(P)-induced immunity and to develop applications for this pathway in crops. We screened immune signaling mutants for loss of NAD(P)-induced HR suppression and found that NAD(P) functions largely in a novel salicylic acid-independent pathway, where NAD(P) treatment of SA-deficient or nonresponsive lines returns cell death during infection to wild type levels. Instead, NAD(P)-induced HR suppression requires members of the immune coreceptor SOMATIC EMBRYOGENESIS RECEPTOR KINASE family and the signal transducer for intracellular nucleotide-binding leucine-rich repeat (NLR) receptors ENHANCED DISEASE SUSCEPTIBILITY 1 and its downstream signaling partners PHYTOALEXIN DEFICIENT 4 and the ACTIVATED DISEASE RESISTANCE 1 family. This work identifies a novel role for EDS1 in NAD(P)-induced cell death suppression during infection and provides a molecular framework for a novel cell survival pathway in plants