Coordinated actions of NLR-assembled and glutamate receptor–like calcium channels in plant effector-triggered immunity

Animal and plant immune systems utilize nucleotide-binding, leucine-rich repeat (NLR) proteins to detect pathogens and translate recognition into host cell death and transcriptional reprogramming for defence. Some Coiled-coil NLRs (CNLs) are proposed to execute cell death autonomously as plasma membrane oligomeric ion channel while Toll-like/Interleukin 1 receptor (TIR) NLRs (TNLs) form a signalling network with helper NLRs containing a CCHeLo domain to confer plant defence. How plant CCHeLo -NLRs confer cell death and induce transcriptional defences is poorly understood. We study this using tobacco where TNLs signal via CCHeLo -NLR N requirement gene 1 (NRG1). Transcriptome data in Nicotiana benthamiana show that glutamate receptor-like channels (GLRs) are highly induced post TNL activation, which can affect cytoplasmic Ca2+ influx. We demonstrate that TNL-activated NRG1 transcriptionally induces GLR2.9a/b and other immune response genes. Oligomerized NRG1 forms Ca2+-permeable cation channel, which cooperates with GLRs at host membranes to promote Ca2+ fluxes, thereby reprogramming cells for resistance and cell death. Our data will advance understanding of how plants control Ca2+ fluxes, and whether this is fundamentally different to CNLs which might be autonomous cell death executioners in plants.