<p>Plant growth and productivity rely on rapid energy management strategies to adapt dynamic environments. Previous work in <i>Arabidopsis thaliana</i> identified a fast-regulatory switch linking cytosolic translation and reactive oxygen species (ROS) signaling, where the protein kinase general control of nonderepressible (GCN)2 is rapidly activated in response to ROS under numerous stresses and phosphorylates the eukaryotic translation initiation factor (eIF)2α as a potential stress mitigation mechanism. Here, we test the hypothesis that the Arabidopsis GCN2-eIF2α’s responses towards the plant defense hormone methyl jasmonate (MeJA) are regulated by light, ROS, and the conserved GCN2 activator protein, general control of non-derepressible 1 (GCN1). We show that eIF2α phosphorylation (P-eIF2α) under MeJA stress requires light and is suppressed by antioxidants and photosynthetic inhibitors. GCN1 is essential for this activation, as <i>gcn1</i> mutant seedlings show reduced P-eIF2α in response to MeJA. Physiologically, both <i>gcn1</i> and <i>gcn2</i> mutants exhibit enhanced sensitivity to MeJA in a primary root growth assay. Surprisingly, despite impaired signaling, <i>gcn2</i> mutants maintain wild-type-like protein synthesis rates under MeJA stress, as shown by polysome profiling and puromycin labeling. Combined, we provide fresh insights into the activation of the Arabidopsis GCN2-eIF2α module in response to MeJA stress by ROS and the GCN1 protein.</p>

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GCN2 is activated by methyl jasmonate through GCN1 and reactive oxygen species in Arabidopsis thaliana

  • Daniel Rincon Diaz,
  • Morgan E. Wynn,
  • Emmanuel Asiedu,
  • Teressa K. Akuoko,
  • Ansul Lokdarshi

摘要

Plant growth and productivity rely on rapid energy management strategies to adapt dynamic environments. Previous work in Arabidopsis thaliana identified a fast-regulatory switch linking cytosolic translation and reactive oxygen species (ROS) signaling, where the protein kinase general control of nonderepressible (GCN)2 is rapidly activated in response to ROS under numerous stresses and phosphorylates the eukaryotic translation initiation factor (eIF)2α as a potential stress mitigation mechanism. Here, we test the hypothesis that the Arabidopsis GCN2-eIF2α’s responses towards the plant defense hormone methyl jasmonate (MeJA) are regulated by light, ROS, and the conserved GCN2 activator protein, general control of non-derepressible 1 (GCN1). We show that eIF2α phosphorylation (P-eIF2α) under MeJA stress requires light and is suppressed by antioxidants and photosynthetic inhibitors. GCN1 is essential for this activation, as gcn1 mutant seedlings show reduced P-eIF2α in response to MeJA. Physiologically, both gcn1 and gcn2 mutants exhibit enhanced sensitivity to MeJA in a primary root growth assay. Surprisingly, despite impaired signaling, gcn2 mutants maintain wild-type-like protein synthesis rates under MeJA stress, as shown by polysome profiling and puromycin labeling. Combined, we provide fresh insights into the activation of the Arabidopsis GCN2-eIF2α module in response to MeJA stress by ROS and the GCN1 protein.