The translation initiation factor eIF2 is phosphorylated to inhibit protein translation through reactive oxygen species under nutrient deficiencies in Arabidopsis

Nitrogen (N), phosphorus (P) or potassium (K) deficiency in plants can lead to a decrease in amino acid and protein synthesis. However, it is unknown how protein translation gets repressed during macronutrient deficiencies. Previous research has shown that general control non-depressible 1 (GCN1) cooperate with GCN2 to phosphorylate the alpha subunit of eukaryotic translation initiation factor (eIF2 alpha). In this study, we observed phosphorylation of eIF2 alpha under N, P, and K deficiencies, which was found to be lost in gcn1. Mutant gcn1 displayed higher sensitivity to macronutrient deficiencies compared to the wild-type (WT). The evidence of in situ reactive oxygen species (ROS) accumulation in leaves indicated that macronutrient starvation triggers ROS production. Treatment with Dimethylthiourea (DMTU), a ROS scavenger, eliminated ROS and reversed eIF2 alpha phosphorylation induced by nutrient deficiency. Moreover, it was discovered that protein translation was reduced under N or K deficiency in the WT but not in gcn1, whereas under P deprivation, protein translation was reduced in both the WT and gcn1. We additionally found that DMTU can partially recover translation inhibition under N or K deprivation. Taken together, it is concluded that GCN1-GCN2-eIF2 alpha pathway is regulated by ROS and is essential for plant survival under macronutrient starvation conditions.