Pattern-recognition receptors are required for NLR-mediated plant immunity

Abstract

23The plant immune system is fundamental to plant survival in natural ecosystems and productivity 24 in crop fields. Substantial evidence supports the prevailing notion that plants possess a two-tiered 25 innate immune system, called pattern-triggered immunity (PTI) and effector-triggered immunity 26 (ETI). PTI is triggered by microbial patterns via cell surface-localized pattern-recognition 27 receptors (PRRs), whereas ETI is activated by pathogen effector proteins via mostly 28 intracellularly-localized receptors called nucleotide-binding, leucine-rich repeat proteins 29 50 from both pathogenic and nonpathogenic microbes. NLRs, on the other hand, are intracellular 51 proteins that sense pathogen-derived effector proteins inside the plant cell and can be further 52 classified into the coiled coil (CC)-type, Toll/interleukin-1 receptor (TIR)-type, or RPW8 (CCR)-53 type, depending on their N-terminal domain 7 . However, PRR-and NLR-mediated signaling 54 pathways result in many similar downstream immune outputs, including defense gene 55 expression, production of ROS and callose deposition at the plant cell wall 8,9 . The underlying 56 reason is not clear and mechanistic relationship between the two immune pathways remains 57 largely enigmatic. Notably, while many PRR signaling components have been identified and 58 anti-pathogen mechanisms described, the downstream signaling events in ETI and how ETI halts 59 pathogen growth still remain poorly understood, despite recent breakthroughs in the 60 understanding of NLR protein structures and activities 10-13 . 61 62 Requirement of PRR/co-receptors for ETI 63 Using Arabidopsis thaliana-Pseudomonas syringae pathosystem, we accidentally discovered a 64 striking and unexpected role of PRR/co-receptors in ETI. Specifically, an "avirulent", ETI-65 eliciting bacterial strain, P. syringae pv. tomato (Pst) DC3000(avrRpt2), which activates RPS2 66 (Resistance to P. syringae 2)-dependent ETI in wild-type Col-0 plants 14,15 , failed to elicit 67 effective ETI in two separate PRR/co-receptor Arabidopsis mutants, fls2/efr/cerk1 (fec) and 68 bak1/bkk1/cerk1 (bbc) mutants, which are mutated in major PRR/co-receptors recognizing 69 bacteria-associated molecular patterns 16 . As shown in Fig. 1a, the fec and bbc mutants did not 70 mount an effective ETI against Pst DC3000(avrRpt2). To determine whether a requirement of 71 PRR/co-receptors for ETI is specific to Pst DC3000(avrRpt2) or is a more general phenomenon, 72 we tested two other ETI-triggering "avirulent" effectors, AvrPphB and AvrRps4, which are 73 recognized by RPS5 17 and RPS4 18 , respectively, in Arabidopsis Col-0 accession. We found that 74 the compromised ETI phenotype in fec and bbc mutants held true for both AvrPphB and 75 AvrRps4 (Extended Data Fig. 1), suggesting a potentially broad role of PRR/co-receptors in ETI 76 pathways. We subsequently focused on AvrRpt2-triggered ETI for in-depth characterization. 77 Hypersensitive response (HR), manifested by fast cell death under high bacterial inoculum, is a...

Genome-Wide Identification, Classification, Characterization, and Expression Analysis of the Wall-Associated Kinase Family during Fruit Development and under Wound Stress in Tomato (Solanum lycopersicum L.)

“…Therefore, wounding provides nutrients to pathogens and facilitates their entry into the tissue and subsequent infection [ 53 ]. During the interaction of plant and pathogen, many plant RLKs, such as FLS2, EFR, and PEPR1 are involved in plant immunity to trigger plant PTI and ETI to anti-pathogens [ 58 ]. Wounding induced WAK-RLKs maybe as an injury signal receptor quickly participated in plant defense response paralleled or combined with other RLKs pathway.…”

Use of virus‐induced gene silencing to characterize genes involved in modulating hypersensitive cell death in maize

“…VPS37-1 colocalized with FLS2 at endosome upon flagellin elicitation and vps37-1 mutants compromised vacuolar sorting of FLS2 and flagellin-triggered stomatal closure, and displayed impaired immunity to the bacterial pathogen P. syringae and to the biotrophic oomycete Hyaloperonospora arabidopsidis(Lu et al, 2012). While FLS2 activation and the resulting MTI do not generally lead to an HR, a strong connection has recently been shown between a functional MTI response and a full ETI response, including HR(Ngou et al, 2020;Yuan et al, 2020).Silencing of VPS37 suppressed Rp1-D21-induced HR in maize(Figure 4a,c). The VPS37 transcript level was reduced by 1.63fold in plants infected with pFoMV-VPS37 compared to control F I G U R E 3 Suppression of Rp1-D21-induced cell death by coexpression of SGT15019 but not SGT9704 in Nicotiana benthamiana.…”

Pattern recognition receptors confer plant salt tolerance via WRKY18/WRKY40 transcription factors

“…This predicts the existence of a critical threshold beyond which further immune activation comes at a cost for salt stress tolerance. Recent studies show that PRR signaling provides an integrating basis for ETI, and that mutual PTI-ETI potentiation is required for effective pathogen resistance (Ngou et al, 2020;Yuan et al, 2020). At present, how NLR signaling exceeds the predicted threshold during ETI remains poorly understood.…”