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 Ca 2+ 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 (CC R ) 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 DIS-EASE 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. RNLsAU : Pleaseconfirmthatallheadinglevelsarerepresentedcorrectly: are central nodes in the plant immune receptor network In Arabidopsis, ADR1 and its 2 paralogs ADR1-LIKE 1 and ADR1-LIKE 2 act redundantly downstream of multiple CNLs and TNLs [7,9,11,12], are required for immune signaling induced at the cell surface by PRRs (see below [5,6]) and basal immunity [7]. Arabidopsis NRG1.1 and NRG1.2 serve as redundant signaling components specifically required for TNLinduced immunity and contribute to basal resistance in the absence of ADR1s [8,9]. Interestingly, functional redundancy has not only been reported within the RNL subfamilies, but also between both subfamilies [11,13]. It is remarkable, however, that in Arabidopsis and Nicotiana benthamiana ADR1s and NRG1s contribute to some sensor NLR-triggered immune responses in an unequally redundant manner. In Arabidopsis, the ADR1 subfamily is predominantly involved in mediating resistance (including transcriptional reprogramming) and the NRG1s in triggering cell death [11]. In contrast, in N. benthamiana NRG1 is sufficient to mediate resistance against tobacco mosaic virus (trigger of the TNL N) or Pseudomonas syringeae (trigger of the TNL Roq1) infections, since knocking out NbADR1 does not affect these resistance responses [13-16]. This may indicate that during evolution, the RNL subfamilies have subfunctionalized in different species or that the preference of the upstream TNLs (see below) for

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