Cytosolic mRNA translation is subject to global and mRNA-specific controls. Phosphorylation of translation initiation factor eIF2 anchors a reversible switch that represses translation globally. The stress-responsive GCN2 kinase is the only known kinase for eIF2 in Arabidopsis. Here we show that conditions that generate reactive oxygen species (ROS) in the chloroplast, such as dark-light transitions, high light, and the herbicide methyl viologen all rapidly activated the GCN2 kinase, whereas mitochondrial and ER stress did not. In addition, GCN2 activation was light dependent and mitigated by photosynthesis inhibitors and ROS quenchers. Accordingly, seedling growth of multiple gcn2 mutant alleles was retarded under conditions of excess light, implicating the GCN2-eIF2 pathway in responses to light and associated ROS. Once activated, the GCN2 kinase preferentially suppressed the ribosome loading of mRNAs for functions such as mitochondrial ATP synthesis, the chloroplast thylakoids, vesicle trafficking, and translation. The transcriptome of gcn2 mutants was sensitized to abiotic stress, including oxidative stress, as well as innate immune responses. Accordingly, gcn2 displayed defects in immune priming by the fungal elicitor, chitin. In conclusion, we provide evidence that reactive oxygen species produced by the photosynthetic apparatus help to activate the highly conserved GCN2 kinase, leading to eIF2 phosphorylation and thus affecting the status of the cytosolic protein synthesis apparatus.

胞质mRNA的翻译受全局和mRNA特异性控制。翻译起始因子eIF2的磷酸化锚定了可逆开关，该开关可全面抑制翻译。应激反应性GCN2激酶是拟南芥中唯一已知的eIF2激酶。在这里，我们显示了在叶绿体中产生活性氧（ROS）的条件，例如暗光过渡，强光和除草剂甲基紫精都可以快速激活GCN2激酶，而线粒体和ER胁迫则不能。此外，GCN2激活是光依赖性的，并通过光合作用抑制剂和ROS猝灭剂减轻。因此，在过量光照条件下，多个gcn2突变等位基因的幼苗生长受到阻碍，这牵涉到GCN2-eIF2途径对光和相关ROS的响应。一旦激活，GCN2激酶优先抑制mRNA的核糖体负载，以实现诸如线粒体ATP合成，叶绿体类囊体，囊泡运输和翻译等功能。gcn2突变体的转录组对非生物胁迫（包括氧化胁迫）和先天免疫应答敏感。因此，gcn2在真菌引发剂几丁质的免疫引发中显示出缺陷。总之，我们提供的证据表明，由光合作用产生的活性氧有助于激活高度保守的GCN2激酶，从而导致eIF2磷酸化，从而影响胞质蛋白合成装置的状态。gcn2突变体的转录组对非生物胁迫（包括氧化胁迫）和先天免疫应答敏感。因此，gcn2在真菌引发剂几丁质的免疫引发中显示出缺陷。总之，我们提供的证据表明，由光合作用产生的活性氧有助于激活高度保守的GCN2激酶，从而导致eIF2磷酸化，从而影响胞质蛋白合成装置的状态。gcn2突变体的转录组对非生物胁迫（包括氧化胁迫）以及先天免疫应答敏感。因此，gcn2在真菌引发剂几丁质的免疫引发中显示出缺陷。总之，我们提供的证据表明，由光合作用产生的活性氧有助于激活高度保守的GCN2激酶，从而导致eIF2磷酸化，从而影响胞质蛋白合成装置的状态。