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<p>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 (eIF2α). In this study, we observed phosphorylation of eIF2α under N, P, and K deficiencies, which was found to be lost in <i>gcn1</i>. Mutant <i>gcn1</i> 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 eIF2α 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 <i>gcn1</i>, whereas under P deprivation, protein translation was reduced in both the WT and <i>gcn1</i>. We additionally found that DMTU can partially recover translation inhibition under N or K deprivation. Taken together, it is concluded that GCN1-GCN2-eIF2α pathway is regulated by ROS and is essential for plant survival under macronutrient starvation conditions.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月23日

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  • Xiaona Cui,
  • Yuanyuan Cao,
  • Mengyang Lv,
  • Shuhao Zhou,
  • Meijun Chen,
  • Chengwei Li,
  • Hairong Zhang

摘要

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 (eIF2α). In this study, we observed phosphorylation of eIF2α 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 eIF2α 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-eIF2α pathway is regulated by ROS and is essential for plant survival under macronutrient starvation conditions.