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- Title
Pathogen effector recognition-dependent association of NRG1 with EDS1 and SAG101 in TNL receptor immunity.
- Authors
Sun, Xinhua; Lapin, Dmitry; Feehan, Joanna M.; Stolze, Sara C.; Kramer, Katharina; Dongus, Joram A.; Rzemieniewski, Jakub; Blanvillain-Baufumé, Servane; Harzen, Anne; Bautor, Jaqueline; Derbyshire, Paul; Menke, Frank L. H.; Finkemeier, Iris; Nakagami, Hirofumi; Jones, Jonathan D. G.; Parker, Jane E.
- Abstract
Plants utilise intracellular nucleotide-binding, leucine-rich repeat (NLR) immune receptors to detect pathogen effectors and activate local and systemic defence. NRG1 and ADR1 "helper" NLRs (RNLs) cooperate with enhanced disease susceptibility 1 (EDS1), senescence-associated gene 101 (SAG101) and phytoalexin-deficient 4 (PAD4) lipase-like proteins to mediate signalling from TIR domain NLR receptors (TNLs). The mechanism of RNL/EDS1 family protein cooperation is not understood. Here, we present genetic and molecular evidence for exclusive EDS1/SAG101/NRG1 and EDS1/PAD4/ADR1 co-functions in TNL immunity. Using immunoprecipitation and mass spectrometry, we show effector recognition-dependent interaction of NRG1 with EDS1 and SAG101, but not PAD4. An EDS1-SAG101 complex interacts with NRG1, and EDS1-PAD4 with ADR1, in an immune-activated state. NRG1 requires an intact nucleotide-binding P-loop motif, and EDS1 a functional EP domain and its partner SAG101, for induced association and immunity. Thus, two distinct modules (NRG1/EDS1/SAG101 and ADR1/EDS1/PAD4) mediate TNL receptor defence signalling. For defence, plants deploy nucleotide binding, leucine-rich repeat (NLR) immune receptors to detect pathogens that signal via modular networks of downstream proteins. Here the authors report rapid induced association of non-interchangeable signalling pathway module components after NLR activation.
- Subjects
IMMUNITY; DISEASE susceptibility; MASS spectrometry; PATHOGENIC microorganisms; IMMUNOPRECIPITATION
- Publication
Nature Communications, 2021, Vol 12, Issue 1, p1
- ISSN
2041-1723
- Publication type
Article
- DOI
10.1038/s41467-021-23614-x