Root-knot nematodes (Meloidogyne spp., RKN) are responsible for extensive crop losses worldwide. For infection, they penetrate plant roots, migrate between plant cells, and establish feeding sites, known as giant cells, in the root pericycle. Previously, we found that nematode perception and early plant responses were similar to those for microbial pathogens and require the BAK1 co-receptor in Arabidopsis thaliana and tomato. To identify additional receptors involved in this process, we implemented a reverse genetic screen for resistance or sensitivity to RKN using Arabidopsis T-DNA alleles of genes encoding transmembrane receptor-like kinases. This screen identified a pair of allelic mutations with enhanced resistance to RKN in a gene we named ENHANCED RESISTANCE TO NEMATODES 1 (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 H₂0₂ accumulation in roots upon RKN elicitor treatments. Elevated MYB51 expression and ROS burst 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. Taken together, our results indicate that ERN1 is an important negative regulator of immunity.

中文翻译：

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G-凝集素受体激酶是拟南芥对根结线虫南方根结线虫免疫的负调节剂

根结线虫 ( Meloidogyne spp., RKN) 是造成世界范围内大量作物损失的原因。对于感染，它们穿透植物根部，在植物细胞之间迁移，并在根周轮中建立称为巨细胞的摄食位点。以前，我们发现线虫感知和早期植物反应与微生物病原体相似，并且需要拟南芥和番茄中的 BAK1 共受体。为了鉴定参与该过程的其他受体，我们使用编码跨膜受体样激酶的基因的拟南芥 T-DNA 等位基因对 RKN 的抗性或敏感性进行了反向遗传筛选。该筛选在我们命名的基因中鉴定了一对对 RKN 具有增强抗性的等位基因突变增强对线虫 1 (ERN1) 的抗性。ERN1编码具有单程跨膜结构域的 G 型凝集素受体激酶 (G-LecRK)。进一步的表征表明，在 RKN 诱导剂处理后，ern1突变体显示出更强的 MAP 激酶激活、防御标记物MYB51水平升高和根中H ₂ 0 ₂积累增强。升高的MYB51表达和ROS突发也在叶中观察到ern1突变体在flg22治疗。的互补ern1.1用35S-或天然启动子驱动ERN1救出RKN感染和增强防御的表型。综上所述，我们的结果表明ERN1是免疫的重要负调节因子。