Small family, big impact: RNL helper NLRs and their importance in plant innate immunity

Abstract

Plants evolved a sophisticated, receptor-based, innate immune system. Cell surface localized pattern recognition (PRR) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors detect pathogen-associated molecular patterns or pathogen-derived effector molecules, respectively, and induce a range of common immune responses. These include Ca2+ fluxes, reactive oxygen species production, and mitogen-activated protein kinase activation [1]. Recent studies have demonstrated an interdependency and mutual potentiation of the 2 receptor systems [2,3]. Based on their N-terminal domains and their phylogeny, NLRs are classified in coiled-coil (CC) domain, Toll-like/interleukin-1 receptor resistance (TIR) domain, and RESISTANCE TO POWDERY MILDEW 8-like CC (CCR) domain containing NLRs, referred to as CNLs, TNLs, and RNLs, respectively [4]. In Arabidopsis thaliana (hereafter Arabidopsis), multiple PRRs and effector sensing NLRs (some CNLs and all tested TNLs) require the presence of RNLs, also termed helper NLRs, to activate full immunity [5,6]. RNLs form a small and evolutionary conserved clade comprised of 2 subfamilies, the ACTIVATED DISEASE RESISTANCE 1 (ADR1) and N REQUIREMENT GENE 1 (NRG1) families that have separated before the divergence of angiosperms [4]. The Arabidopsis genome bares 3 ADR1 and 2 NRG1 full-length genes required for full immunity [7–9]. Although RNLs represent only a relatively small part of the NLR gene repertoire in most angiosperms [4,10], they are of outmost importance for plants to fight off invading pathogens. Here, we highlight recent findings of how RNLs function during immunity and discuss mechanisms of RNL activation.