Help wanted: helper NLRs and plant immune responses

Plant nucleotide-binding domain and leucine-rich repeat-containing (NLR) proteins function as intracellular receptors in response to pathogens and activate effector-triggered immune responses (ETI). The activation of some sensor NLRs (sNLR) by their corresponding pathogen effector is well studied. However, the mechanisms by which the recently defined helper NLRs (hNLR) function to transduce sNLR activation into ETI-associated cell death and disease resistance remains poorly understood. We briefly summarize recent examples of sNLR activation and we then focus on hNLR requirements in sNLR-initiated immune responses. We further discuss how shared sequence homology with fungal self-incompatibility proteins and the mammalian mixed lineage kinase domain like pseudokinase (MLKL) proteins informs a plausible model for the structure and function of an ancient clade of plant hNLRs, called RNLs

Two unequally redundant "helper" immune receptor families mediate Arabidopsis thaliana intracellular "sensor" immune receptor functions

Plant nucleotide-binding (NB) leucine-rich repeat (LRR) receptor (NLR) proteins function as intracellular immune receptors that perceive the presence of pathogen-derived virulence proteins (effectors) to induce immune responses. The 2 major types of plant NLRs that "sense"pathogen effectors differ in their N-terminal domains: these are Toll/interleukin-1 receptor resistance (TIR) domain-containing NLRs (TNLs) and coiled-coil (CC) domain-containing NLRs (CNLs). In many angiosperms, the RESISTANCE TO POWDERY MILDEW 8 (RPW8)-CC domain containing NLR (RNL) subclass of CNLs is encoded by 2 gene families, ACTIVATED DISEASE RESISTANCE 1 (ADR1) and N REQUIREMENT GENE 1 (NRG1), that act as "helper"NLRs during multiple sensor NLR-mediated immune responses. Despite their important role in sensor NLR-mediated immunity, knowledge of the specific, redundant, and synergistic functions of helper RNLs is limited. We demonstrate that the ADR1 and NRG1 families act in an unequally redundant manner in basal resistance, effector-triggered immunity (ETI) and regulation of defense gene expression. We define RNL redundancy in ETI conferred by some TNLs and in basal resistance against virulent pathogens. We demonstrate that, in Arabidopsis thaliana, the 2 RNL families contribute specific functions in ETI initiated by specific CNLs and TNLs. Time-resolved whole genome expression profiling revealed that RNLs and "classical"CNLs trigger similar transcriptome changes, suggesting that RNLs act like other CNLs to mediate ETI downstream of sensor NLR activation. Together, our genetic data confirm that RNLs contribute to basal resistance, are fully required for TNL signaling, and can also support defense activation during CNL-mediated ETI