Abstract

Both animals and plants utilize nucleotide-binding leucine-rich repeat immune receptors (NLRs) to perceive the presence of pathogen-derived molecules and induce immune responses. NLR genes are far more abundant and diverse in higher plants. Interestingly, truncated NLRs, which lack one or more of the canonical domains, are also commonly encoded in plant genomes. However, little is known about their functions, especially regarding the N-terminally truncated ones. Here, we show that Arabidopsis thaliana (A. thaliana) N-terminally truncated helper NLR gene NRG1C (N REQUIREMENT GENE 1) is highly induced upon pathogen infection and in autoimmune mutants. The immune response and cell death conferred by some TIR (Toll/interleukin-1 receptor)-type NLRs (TNLs) are compromised in the NRG1C overexpression lines. Detailed genetic analysis revealed that NRG1C antagonizes the immunity mediated by its full-length neighbors NRG1A and NRG1B. Biochemical tests indicate that NRG1C possibly interferes with the EDS1-SAG101 complex, which likely signals together with NRG1A/1B. Interestingly, Brassicaceae NRG1Cs are functionally exchangeable, and the Nicotiana benthamiana (N. benthamiana) N-terminally truncated helper NLR NRG2 antagonizes NRG1 in tobacco. Together, our study uncovers an unexpected negative role of N-terminally truncated helper NLRs in different plants.