Howard Hughes Medical Institute, Department of Biology, Duke University, Durham, NC 27708, USA.
Howard Hughes Medical Institute, Department of Biology, Duke University, Durham, NC 27708, USA.
Cell Host Microbe. 2023 Mar 8;31(3):334-342.e5. doi: 10.1016/j.chom.2023.01.014. Epub 2023 Feb 17.
The recognition of pathogen effectors by their cognate nucleotide-binding leucine-rich repeat (NLR) receptors activates effector-triggered immunity (ETI) in plants. ETI is associated with correlated transcriptional and translational reprogramming and subsequent death of infected cells. Whether ETI-associated translation is actively regulated or passively driven by transcriptional dynamics remains unknown. In a genetic screen using a translational reporter, we identified CDC123, an ATP-grasp protein, as a key activator of ETI-associated translation and defense. During ETI, an increase in ATP concentration facilitates CDC123-mediated assembly of the eukaryotic translation initiation factor 2 (eIF2) complex. Because ATP is required for the activation of NLRs as well as the CDC123 function, we uncovered a possible mechanism by which the defense translatome is coordinately induced during NLR-mediated immunity. The conservation of the CDC123-mediated eIF2 assembly suggests its possible role in NLR-mediated immunity beyond plants.
病原体效应物被其同源核苷酸结合富含亮氨酸重复(NLR)受体识别,从而激活植物中的效应物触发的免疫(ETI)。ETI 与相关的转录和翻译重编程以及随后受感染细胞的死亡有关。ETI 相关的翻译是主动调节还是被动地由转录动力学驱动尚不清楚。在使用翻译报告基因的遗传筛选中,我们鉴定出 CDC123(一种 ATP 捕获蛋白)是 ETI 相关翻译和防御的关键激活因子。在 ETI 期间,ATP 浓度的增加有助于 CDC123 介导的真核翻译起始因子 2(eIF2)复合物的组装。由于 ATP 是 NLR 激活以及 CDC123 功能所必需的,因此我们揭示了 NLR 介导的免疫过程中防御转译组协调诱导的可能机制。CDC123 介导的 eIF2 组装的保守性表明,它在 NLR 介导的免疫中可能具有超越植物的作用。