Abstract
ABSTRACTCell surface pattern recognition receptors (PRRs) activate immune responses that can include the hypersensitive cell death. However, the pathways that link PRRs to the cell death response are poorly understood. Here, we show that the cell surface receptor-like protein Cf-4 requires the intracellular nucleotide-binding domain leucine-rich repeat containing receptor (NLR) NRC3 to trigger a confluent cell death response upon detection of the fungal effector Avr4 in leaves of Nicotiana benthamiana. This NRC3 activity requires an intact N-terminal MADA motif, a conserved signature of coiled-coil (CC)-type plant NLRs that is required for resistosome-mediated immune responses. A chimeric protein with the N-terminal α1 helix of Arabidopsis ZAR1 swapped into NRC3 retains the capacity to mediate Cf-4 hypersensitive cell death. Pathogen effectors acting as suppressors of NRC3 can suppress Cf-4-triggered hypersensitive cell-death. Our findings link the NLR resistosome model to the hypersensitive cell death caused by a cell surface PRR.
Publisher
Cold Spring Harbor Laboratory
Reference61 articles.
1. An N-terminal motif in NLR immune receptors is functionally conserved across distantly related plant species
2. NLR singletons, pairs, and networks: evolution, assembly, and regulation of the intracellular immunoreceptor circuitry of plants
3. An RLP23–SOBIR1–BAK1 complex mediates NLP-triggered immunity;Nat. Plants,2015
4. SOBIR1 requires the GxxxG dimerization motif in its transmembrane domain to form constitutive complexes with receptor-like proteins;Mol. Plant Pathol,2016
5. Bi, G. , Su, M. , Li, N. , et al. (2021) The ZAR1 resistosome is a calcium-permeable channel triggering plant immune signaling. Cell, 0. Available at: https://www.cell.com/cell/abstract/S0092-8674(21)00600-0
Cited by
12 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献