Two genetically linked Arabidopsis TIR-type NLRs are required for immunity and interact with NLRs encoded in a segmentally duplicated genomic region

Plant nucleotide-binding leucine-rich repeat (NLR) immune receptors detect pathogen-secreted effectors inside host cells and induce a robust immune response, typically involving hypersensitive cell death. NLR genes are often genetically linked and can function as pairs or within larger NLR networks. We previously showed that the truncated Toll/Interleukin-1 Receptor (TIR)-type NLR TIR-NB13 (TN13) is required for resistance of Arabidopsis to Pseudomonas syringae pv. tomato ( Pst ) DC3000 lacking the type-III effector proteins AvrPto and AvrPtoB. TN13 is genetically linked to a full length TIR-NB-LRR ( TNL ) gene on chromosome 3. Here, we show that TN13, and its genetically linked TNL both localize to the ER membrane via N-terminal transmembrane domains, are required for resistance to Pst DC3000 (ΔAvrPto/AvrPtoB) and interact with each other in transient expression assays in Nicotiana benthamiana . In contrast to TN13, the full length TNL, which we named TN13-INTERACTING TNL1 (TNT1), induces an autoactive cell death response when expressed in N. benthamiana that depends on an atypical MHV motif in its NB-ARC domain, as well as the EDS1/SAG101/NRG1 module. TN13 and TNT1 furthermore interact with phylogenetically related NLRs encoded by a segmentally duplicated region on chromosome 5. Our data suggest that both TN13 and the genetically linked TNT1 could be part of a larger TIR-type NLR immune regulatory network, in which TNT1 contributes to basal immunity and might function as an autoactive death switch to induce cell death upon pathogen detection.