Upon stress, eukaryotes typically reprogram their translatome through GCN2-mediated phosphorylation of the eukaryotic translation initiation factor, eIF2α, to inhibit general translation initiation while selectively translating essential stress regulators. Unexpectedly, in plants, pattern-triggered immunity (PTI) and response to other environmental stresses occur independently of the GCN2/eIF2α pathway. Here, we show that while PTI induces mRNA decapping to inhibit general translation, defense mRNAs with a purine-rich element (“R-motif”) are selectively translated using R-motif as an internal ribosome entry site (IRES). R-motif-dependent translation is executed by poly(A)-binding proteins (PABPs) through preferential association with the PTI-activating eIFiso4G over the repressive eIF4G. Phosphorylation by PTI regulators mitogen-activated protein kinase 3 and 6 (MPK3/6) inhibits eIF4G’s activity while enhancing PABP binding to the R-motif and promoting eIFiso4G-mediated defense mRNA translation, establishing a link between PTI signaling and protein synthesis. Given its prevalence in both plants and animals, the PABP/R-motif translation initiation module may have a broader role in reprogramming the stress translatome.

在应激时，真核生物通常通过 GCN2 介导的真核翻译起始因子 eIF2α 磷酸化来重新编程其翻译组，以抑制一般翻译起始，同时选择性地翻译必需的应激调节因子。出乎意料的是，在植物中，模式触发免疫（PTI）和对其他环境胁迫的反应独立于 GCN2/eIF2α 途径而发生。在这里，我们表明，虽然 PTI 诱导 mRNA 脱帽以抑制一般翻译，但使用 R 基序作为内部核糖体进入位点 (IRES) 选择性翻译具有富含嘌呤元件（“R-基序”）的防御 mRNA。R 基序依赖性翻译是由多聚腺苷酸结合蛋白 (PABP) 通过优先与 PTI 激活 eIFiso4G 而非抑制性 eIF4G 关联来执行。PTI 调节剂丝裂原激活蛋白激酶 3 和 6 (MPK3/6) 的磷酸化可抑制 eIF4G 的活性，同时增强 PABP 与 R 基序的结合并促进 eIFiso4G 介导的防御 mRNA 翻译，从而在 PTI 信号传导和蛋白质合成之间建立联系。鉴于其在植物和动物中的普遍存在，PABP/R-基序翻译起始模块可能在重编程应激翻译组方面发挥更广泛的作用。