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<p>Cells and organisms frequently experience starvation. To survive, they mount an evolutionarily conserved stress response. A vital component in the mammalian starvation response is eukaryotic elongation factor 2 (eEF2) kinase (eEF2K), which suppresses translation in starvation by phosphorylating and inactivating the translation elongation driver eEF2. <i>C. elegans</i> EFK-1/eEF2K phosphorylates EEF-2/eEF2 on a conserved residue and is required for starvation survival, but how it promotes survival remains unclear. Surprisingly, we found that eEF2 phosphorylation is unchanged in starved <i>C. elegans</i> and EFK-1’s kinase activity is dispensable for starvation survival, suggesting that <i>efk-1</i> promotes survival via a noncanonical pathway. We show that <i>efk-1</i> upregulates transcription of DNA repair pathways, nucleotide excision repair (NER) and base excision repair (BER), to promote starvation survival. Furthermore, <i>efk-1</i> suppresses oxygen consumption and ROS production in starvation to prevent oxidative stress. Thus, <i>efk-1</i> enables starvation survival by protecting animals from starvation-induced oxidative damage through an EEF-2-independent pathway.</p>

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Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年2月18日

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  • Junran Yan,
  • Forum Bhanshali,
  • Chiaki Shuzenji,
  • Tsultrim T. Mendenhall,
  • Shane K. B. Taylor,
  • Glafira Ermakova,
  • Xuanjin Cheng,
  • Pamela Bai,
  • Gahan Diwan,
  • Donna Seraj,
  • Joel N. Meyer,
  • Poul H. Sorensen,
  • Jessica H. Hartman,
  • Stefan Taubert

摘要

Cells and organisms frequently experience starvation. To survive, they mount an evolutionarily conserved stress response. A vital component in the mammalian starvation response is eukaryotic elongation factor 2 (eEF2) kinase (eEF2K), which suppresses translation in starvation by phosphorylating and inactivating the translation elongation driver eEF2. C. elegans EFK-1/eEF2K phosphorylates EEF-2/eEF2 on a conserved residue and is required for starvation survival, but how it promotes survival remains unclear. Surprisingly, we found that eEF2 phosphorylation is unchanged in starved C. elegans and EFK-1’s kinase activity is dispensable for starvation survival, suggesting that efk-1 promotes survival via a noncanonical pathway. We show that efk-1 upregulates transcription of DNA repair pathways, nucleotide excision repair (NER) and base excision repair (BER), to promote starvation survival. Furthermore, efk-1 suppresses oxygen consumption and ROS production in starvation to prevent oxidative stress. Thus, efk-1 enables starvation survival by protecting animals from starvation-induced oxidative damage through an EEF-2-independent pathway.