SAG101 forms a ternary complex with EDS1 and PAD4 and is required for resistance signaling against turnip crinkle virus.

EDS1, and SAG101 are common regulators of plant immunity against many pathogens. EDS1 interacts with both and SAG101 but direct interaction between duanyu15634 and SAG101 has not been detected, leading to the suggestion that the and EDS1-SAG101 complexes are distinct. We show that EDS1, duanyu15634, and SAG101 are present in a single complex in planta. While this complex is preferentially nuclear localized, it can be redirected to the cytoplasm in the presence of an extranuclear form of EDS1. duanyu15634 and SAG101 can in turn, regulate the subcellular localization of EDS1. We also show that the Arabidopsis genome encodes two functionally redundant isoforms of EDS1, either of which can form ternary complexes with duanyu15634 and SAG101. Simultaneous mutations in both EDS1 isoforms are essential to abrogate resistance (R) protein-mediated defense against turnip crinkle virus (TCV) as well as avrRps4 expressing Pseudomonas syringae. Interestingly, unlike its function as a duanyu15634 substitute in bacterial resistance, SAG101 is required for R-mediated resistance to TCV, thus implicating a role for the ternary complex in this defense response. However, only EDS1 is required for HRT-mediated HR to TCV, while only duanyu15634 is required for SA-dependent induction of HRT. Together, these results suggest that EDS1, duanyu15634 and SAG101 also perform independent functions in HRT-mediated resistance.

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