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）富含亮氨酸的重复（LRR）受体（NLR）蛋白起细胞内免疫受体的作用，可感知病原体衍生的毒性蛋白（效应子）的存在，从而诱导免疫反应。“感知”病原体效应子的两种主要植物NLR类型在其N末端域上有所不同：它们是Toll /白介素1受体抗性（TIR）域的NLR（TNL）和盘绕线圈（CC）的域NLR（CNL）。在许多被子植物中，含有CNL的NLR（RNL）子类的POWLERY MILDEW 8（RPW8）-CC域的抗性由2个基因家族编码，即活化疾病抗性1（ADR1）和N需求基因1（NRG1）），在多传感器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，效应子触发的免疫（ETI）和防御基因表达的调节中以不相等的冗余方式起作用。我们定义了一些TNL赋予的ETI中的RNL冗余，以及针对毒性病原体的基础抗性。我们证明，在拟南芥中，这2个RNL系列在由特定CNL和TNL发起的ETI中贡献特定功能。时间分辨的全基因组表达谱显示，RNL和“经典” CNL触发相似的转录组变化，表明RNL像其他CNL一样，在传感器NLR激活下游介导ETI。在一起，我们的遗传数据证实RNL有助于基础抵抗力，是TNL信号转导所完全需要的，并且还可以支持CNL介导的ETI过程中的防御激活。