bioRxiv · 10.1101/2024.03.20.585993
Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans
Abstract
Cells and organisms frequently experience starvation. To adapt and 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 responds to starvation by phosphorylating and inactivating the translation elongation driver eEF2, thus shutting down translation and facilitating survival. 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, suggesting that efk-1 promotes survival via a noncanonical pathway. We show that efk-1 upregulates transcription of the 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 a translation-independent pathway.
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Yan, J., Bhanshali, F., Shuzenji, C., Mendenhall, T. T., Cheng, X., Bai, P., Diwan, G., Seraj, D., Meyer, J. N., Sorensen, P. H., Hartman, J. H., Taubert, S.. 2024-03-24. Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans. https://doi.org/10.1101/2024.03.20.585993
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