Oligomerization of a plant helper NLR requires cell-surface and intracellular immune receptor activation

Plant disease resistance involves both detection of microbial molecular patterns by cell-surface pattern recognition receptors and detection of pathogen effectors by intracellular NLR immune receptors. NLRs are classified as sensor NLRs, involved in effector detection, or helper NLRs required for se...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2023-03, Vol.120 (11), p.e2210406120-e2210406120
Main Authors: Feehan, Joanna M, Wang, Junli, Sun, Xinhua, Choi, Jihyeon, Ahn, Hee-Kyung, Ngou, Bruno Pok Man, Parker, Jane E, Jones, Jonathan D G
Format: Article
Language:English
Subjects:
Biological Sciences
Cell Membrane
Cell surface
Disease Resistance
Immunity
Intracellular
Intracellular signalling
Lipase
Microorganisms
Oligomerization
Pattern recognition
Pattern recognition receptors
Plant Diseases
Plant Immunity
Potentiation
Receptor mechanisms
Receptors
Receptors, Immunologic - genetics
Sensors
Signaling
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Summary:Plant disease resistance involves both detection of microbial molecular patterns by cell-surface pattern recognition receptors and detection of pathogen effectors by intracellular NLR immune receptors. NLRs are classified as sensor NLRs, involved in effector detection, or helper NLRs required for sensor NLR signaling. TIR-domain-containing sensor NLRs (TNLs) require helper NLRs NRG1 and ADR1 for resistance, and helper NLR activation of defense requires the lipase-domain proteins EDS1, SAG101, and PAD4. Previously, we found that NRG1 associates with EDS1 and SAG101 in a TNL activation-dependent manner [X. Sun , , 3335 (2021)]. We report here how the helper NLR NRG1 associates with itself and with EDS1 and SAG101 during TNL-initiated immunity. Full immunity requires coactivation and mutual potentiation of cell-surface and intracellular immune receptor-initiated signaling [B. P. M. Ngou, H.-K. Ahn, P. Ding, J. D. G. Jones, , 110-115 (2021), M. Yuan  ,  , 105-109 (2021)]. We find that while activation of TNLs is sufficient to promote NRG1-EDS1-SAG101 interaction, the formation of an oligomeric NRG1-EDS1-SAG101 resistosome requires the additional coactivation 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.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.2210406120