Center for Plant Molecular Biology, Eberhard Karls University of Tübingen, Tübingen, Germany.
Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States of America.
PLoS Biol. 2020 Sep 14;18(9):e3000783. doi: 10.1371/journal.pbio.3000783. eCollection 2020 Sep.
Plant nucleotide-binding (NB) leucine-rich repeat (LRR) receptor (NLR) proteins function as intracellular immune receptors that perceive the presence of pathogen-derived virulence proteins (effectors) to induce immune responses. The 2 major types of plant NLRs that "sense" pathogen effectors differ in their N-terminal domains: these are Toll/interleukin-1 receptor resistance (TIR) domain-containing NLRs (TNLs) and coiled-coil (CC) domain-containing NLRs (CNLs). In many angiosperms, the RESISTANCE TO POWDERY MILDEW 8 (RPW8)-CC domain containing NLR (RNL) subclass of CNLs is encoded by 2 gene families, ACTIVATED DISEASE RESISTANCE 1 (ADR1) and N REQUIREMENT GENE 1 (NRG1), that act as "helper" NLRs during multiple sensor NLR-mediated immune responses. Despite their important role in sensor NLR-mediated immunity, knowledge of the specific, redundant, and synergistic functions of helper RNLs is limited. We demonstrate that the ADR1 and NRG1 families act in an unequally redundant manner in basal resistance, effector-triggered immunity (ETI) and regulation of defense gene expression. We define RNL redundancy in ETI conferred by some TNLs and in basal resistance against virulent pathogens. We demonstrate that, in Arabidopsis thaliana, the 2 RNL families contribute specific functions in ETI initiated by specific CNLs and TNLs. Time-resolved whole genome expression profiling revealed that RNLs and "classical" CNLs trigger similar transcriptome changes, suggesting that RNLs act like other CNLs to mediate ETI downstream of sensor NLR activation. Together, our genetic data confirm that RNLs contribute to basal resistance, are fully required for TNL signaling, and can also support defense activation during CNL-mediated ETI.
植物核苷酸结合（NB）富含亮氨酸重复（LRR）受体（NLR）蛋白作为细胞内免疫受体，可感知病原体衍生的毒力蛋白（效应物）的存在，从而诱导免疫反应。识别病原体效应物的 2 种主要类型的植物 NLR 在其 N 端结构域上有所不同：一种是含 Toll/白细胞介素-1 受体抗性（TIR）结构域的 NLR（TNLs），另一种是含卷曲螺旋（CC）结构域的 NLR（CNLs）。在许多被子植物中，含 RESISTANCE TO POWDERY MILDEW 8（RPW8）-CC 结构域的 NLR（RNL）亚类 CNLs 由 2 个基因家族编码，即 ACTIVATED DISEASE RESISTANCE 1（ADR1）和 N REQUIREMENT GENE 1（NRG1），它们在多种传感器 NLR 介导的免疫反应中充当“辅助” NLR。尽管它们在传感器 NLR 介导的免疫中起着重要作用，但对辅助 RNL 的特定、冗余和协同功能的了解有限。我们证明 ADR1 和 NRG1 家族在基础抗性、效应物触发的免疫（ETI）和防御基因表达调控中以不均等冗余的方式发挥作用。我们定义了一些 TNLs 赋予的 ETI 中的 RNL 冗余性以及对强毒病原体的基础抗性中的 RNL 冗余性。我们证明，在拟南芥中，2 个 RNL 家族在由特定 CNLs 和 TNLs 引发的 ETI 中发挥特定功能。时间分辨的全基因组表达谱分析表明，RNLs 和“经典”CNLs 触发相似的转录组变化，这表明 RNLs 像其他 CNLs 一样在传感器 NLR 激活下游介导 ETI。总之，我们的遗传数据证实 RNLs 有助于基础抗性，是 TNL 信号所必需的，并且还可以在 CNL 介导的 ETI 期间支持防御激活。
