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

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 and Stefan Taubert ()
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Junran Yan: 950 W 28 th Ave
Forum Bhanshali: 950 W 28 th Ave
Chiaki Shuzenji: 950 W 28 th Ave
Tsultrim T. Mendenhall: 173 Ashley Ave
Shane K. B. Taylor: 950 W 28 th Ave
Glafira Ermakova: 950 W 28 th Ave
Xuanjin Cheng: 950 W 28 th Ave
Pamela Bai: 950 W 28 th Ave
Gahan Diwan: 950 W 28 th Ave
Donna Seraj: 950 W 28 th Ave
Joel N. Meyer: Duke University
Poul H. Sorensen: 675 W 10th Ave
Jessica H. Hartman: 173 Ashley Ave
Stefan Taubert: 950 W 28 th Ave

Nature Communications, 2025, vol. 16, issue 1, 1-22

Abstract: Abstract 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.

Date: 2025
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DOI: 10.1038/s41467-025-56766-1

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