Department of Plant-Microbe Interactions, Max-Planck Institute for Plant Breeding Research, 50829 Cologne, Germany.
Cellular Networks and Systems Biology, CECAD, University of Cologne, Cologne 50931, Germany.
Plant Cell. 2019 Oct;31(10):2430-2455. doi: 10.1105/tpc.19.00118. Epub 2019 Jul 16.
Plant nucleotide binding/leucine-rich repeat (NLR) immune receptors are activated by pathogen effectors to trigger host defenses and cell death. Toll-interleukin 1 receptor domain NLRs (TNLs) converge on the ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) family of lipase-like proteins for all resistance outputs. In Arabidopsis () TNL-mediated immunity, EDS1 heterodimers with PHYTOALEXIN DEFICIENT4 (PAD4) transcriptionally induced basal defenses. EDS1 uses the same surface to interact with PAD4-related SENESCENCE-ASSOCIATED GENE101 (SAG101), but the role of EDS1-SAG101 heterodimers remains unclear. We show that EDS1-SAG101 functions together with N REQUIRED GENE1 (NRG1) coiled-coil domain helper NLRs as a coevolved TNL cell death-signaling module. EDS1-SAG101-NRG1 cell death activity is transferable to the Solanaceous species and cannot be substituted by EDS1-PAD4 with NRG1 or EDS1-SAG101 with endogenous NRG1. Analysis of EDS1-family evolutionary rate variation and heterodimer structure-guided phenotyping of EDS1 variants and PAD4-SAG101 chimeras identify closely aligned ɑ-helical coil surfaces in the EDS1-SAG101 partner C-terminal domains that are necessary for reconstituted TNL cell death signaling. Our data suggest that TNL-triggered cell death and pathogen growth restriction are determined by distinctive features of EDS1-SAG101 and EDS1-PAD4 complexes and that these signaling machineries coevolved with other components within plant species or clades to regulate downstream pathways in TNL immunity.
植物核苷酸结合/富含亮氨酸重复（NLR）免疫受体被病原体效应物激活，引发宿主防御和细胞死亡。Toll-白细胞介素 1 受体结构域 NLR（TNLs）通过增强疾病易感性 1（EDS1）家族的脂肪酶样蛋白汇聚在一起，以产生所有抗性输出。在拟南芥中，TNL 介导的免疫中，EDS1 异二聚体与 PHYTOALEXIN DEFICIENT4（PAD4）转录诱导基础防御。EDS1 使用相同的表面与 PAD4 相关的 SENESCENCE-ASSOCIATED GENE101（SAG101）相互作用，但 EDS1-SAG101 异二聚体的作用仍不清楚。我们表明，EDS1-SAG101 与 N REQUIRED GENE1（NRG1）卷曲螺旋结构域辅助 NLR 一起作为共同进化的 TNL 细胞死亡信号模块发挥作用。EDS1-SAG101-NRG1 细胞死亡活性可转移到茄科物种 ，并且不能被 NRG1 与 EDS1-PAD4 或 EDS1-SAG101 与内源性 NRG1 取代。EDS1 家族进化率变化分析和 EDS1 变体和 PAD4-SAG101 嵌合体的异二聚体结构指导表型分析确定了在 EDS1-SAG101 伴侣 C 端结构域中紧密对齐的 ɑ-螺旋卷曲表面，这对于重建的 TNL 细胞死亡信号是必需的。我们的数据表明，TNL 触发的细胞死亡和病原体生长限制取决于 EDS1-SAG101 和 EDS1-PAD4 复合物的独特特征，并且这些信号机制与植物物种或进化枝内的其他成分共同进化，以调节 TNL 免疫中的下游途径。
