Postdoctoral Fellow Carnegie Institution of Science, Department of Plant Biology Stanford, California
Body of Abstract: Plant disease resistance involves both detection of microbes by cell-surface pattern recognition receptors and effectors by intracellular NLR immune receptors. Sensor NLRs detect effectors with helper NLRs that are required for sensor NLR signaling. Resistance in plants mediated by TIR domain-containing sensor NLRs (TNLs) requires the helper NLRs NRG1 and ADR1 and their lipase domain-containing signalling partners EDS1, SAG101, and PAD4. Previously, we found that NRG1 associates with EDS1 and SAG101 in a TNL activation-dependent manner. Here we show that the helper NLR NRG1 associates with itself and with EDS1 and SAG101 during TNL-initiated immunity. However, full immunity requires co-activation and mutual potentiation of cell-surface and intracellular immune receptor initiated signaling. We find that while activation of TNLs is sufficient to promote NRG1-EDS1-SAG101 interaction, formation of an oligomeric NRG1-EDS1-SAG101 resistosome requires the additional co-activation of cell-surface receptor-initiated defense. These data suggest that NRG1-EDS1-SAG101 resistosome formation in vivo is part of the mechanism that links intracellular and cell-surface receptor signaling pathways.