Dissecting the Role of SAG101 in Extracellular NAD(P)+-Mediated Immune Signaling

Abstract

Plants are the primary source of food for all animals, but they are often infected by microbial pathogens, which reduces crop yield and threatens global food security. Therefore, plants have evolved sophisticated defense mechanisms to fend off microbial infections. EDS1, PAD4, and SAG101 are well-characterized plant immune regulators. While the EDS1-PAD4 complex was proven to be necessary for extracellular NAD(P) [eNAD(P)]-mediated immune signaling, the function of the EDS1-SAG101 complex in this pathway has yet to be determined. This research aimed to determine the necessity of SAG101 in the process of eNAD(P) signaling. Our hypothesis was that SAG101 formed a complex with EDS1 to carry out a necessary role in eNAD(P) signaling. Arabidopsis thaliana T-DNA insertion lines SALK_022911C and SALK_030411C were genotyped, and SALK_022911C was identified as a sag101 homozygous mutant. NAD(P)-induced immune responses in the sag101 mutant were compared to those in the eds1 and pad4 mutants. Exogenously applied NAD(P) induced expression of the defense marker genes, FMO1 and ALD1, as well as resistance to the bacterial pathogen Pseudomonas syringae pv. maculicola ES4326 in sag101. However, this induction was completely blocked in eds1 and pad4. These results demonstrate that the EDS1-SAG101 complex is not involved in the eNAD(P) signaling pathway and supports the model that the EDS1-PAD4 and EDS1-SAG101 complexes function differently in plant immunity.