A G-type lectin receptor kinase negatively regulates Arabidopsis immunity against root-knot nematodes

Abstract

Root-knot nematodes (Meloidogyne spp., RKN) are responsible for extensive crop losses worldwide. During infection, they penetrate plant roots, migrate between plant cells, and establish feeding sites, known as giant cells, near the root vasculature. Previously, we found that nematode perception and early responses in plants were similar to those of microbial pathogens and required the BRI1-ASSOCIATED KINASE1/SOMATIC EMBRYOGENESIS RECEPTOR KINASE3 (BAK1/SERK3) coreceptor in Arabidopsis (Arabidopsis thaliana) and tomato (Solanum lycopersicum). Here, we implemented a reverse genetic screen for resistance or sensitivity to RKN using Arabidopsis T-DNA alleles of genes encoding transmembrane receptor-like kinases to identify additional receptors involved in this process. This screen identified a pair of allelic mutations with enhanced resistance to RKN in a gene we named ENHANCED RESISTANCE TO NEMATODES1 (ERN1). ERN1 encodes a G-type lectin receptor kinase (G-LecRK) with a single-pass transmembrane domain. Further characterization showed that ern1 mutants displayed stronger activation of MAP kinases, elevated levels of the defense marker MYB51, and enhanced H2O2 accumulation in roots upon RKN elicitor treatments. Elevated MYB51 expression and ROS bursts were also observed in leaves of ern1 mutants upon flg22 treatment. Complementation of ern1.1 with 35S- or native promotor-driven ERN1 rescued the RKN infection and enhanced defense phenotypes. Our results indicate that ERN1 is an important negative regulator of immunity.

LORE receptor homomerization is required for 3‐hydroxydecanoic acid‐induced immune signaling and determines the natural variation of immunosensitivity within the Arabidopsis genus

“…Apart from SRKs, only a few SD‐RLKs have been described in more detail. They are involved in plant–pathogen interactions and symbiosis or abiotic stress responses (Walker & Zhang, 1990; Tobias et al ., 1992; Tobias & Nasrallah, 1996; Chen et al ., 2006, 2013; Kim et al ., 2009a,b; Gilardoni et al ., 2011; Cheng et al ., 2013; X. L. Sun et al ., 2013; Trontin et al ., 2014; Ranf et al ., 2015; Zou et al ., 2015; Fan et al ., 2018; Schnepf et al ., 2018; Kutschera et al ., 2019; Labbé et al ., 2019; Park et al ., 2019; Jinjun et al ., 2020; Pan et al ., 2020; Sun et al ., 2020; Liu et al ., 2021; Mondal et al ., 2021; Schellenberger et al ., 2021; Kato et al ., 2022; Ma et al ., 2022; Bao et al ., 2023; Pi et al ., 2023; Shrestha et al ., 2023; Zhou et al ., 2023). Although a growing number of members of the large SD‐RLK sub‐family are being characterized, their ligands, receptor complex formation, and downstream signaling mechanisms remain largely unknown.…”