PUBLICATION

ROS-induced ribosome impairment underlies ZAKα-mediated metabolic decline in obesity and aging

Authors
Snieckute, G., Ryder, L., Vind, A.C., Wu, Z., Arendrup, F.S., Stoneley, M., Chamois, S., Martinez-Val, A., Leleu, M., Dreos, R., Russell, A., Gay, D.M., Genzor, A.V., Choi, B.S., Basse, A.L., Sass, F., Dall, M., Dollet, L.C.M., Blasius, M., Willis, A.E., Lund, A.H., Treebak, J.T., Olsen, J.V., Poulsen, S.S., Pownall, M.E., Jensen, B.A.H., Clemmensen, C., Gerhart-Hines, Z., Gatfield, D., Bekker-Jensen, S.
ID
ZDB-PUB-231208-7
Date
2023
Source
Science (New York, N.Y.)   382: eadf3208eadf3208 (Journal)
Registered Authors
Pownall, Betsy
Keywords
none
MeSH Terms
  • Mice, Knockout
  • Mice
  • Aging*/metabolism
  • Stress, Physiological*
  • Protein Biosynthesis
  • Zebrafish
  • Obesity*/metabolism
  • Animals
  • Reactive Oxygen Species*/metabolism
  • Ribosomes*/metabolism
  • MAP Kinase Kinase Kinase 3*/genetics
  • MAP Kinase Kinase Kinase 3*/metabolism
PubMed
38060659 Full text @ Science
Abstract
The ribotoxic stress response (RSR) is a signaling pathway in which the p38- and c-Jun N-terminal kinase (JNK)-activating mitogen-activated protein kinase kinase kinase (MAP3K) ZAKα senses stalling and/or collision of ribosomes. Here, we show that reactive oxygen species (ROS)-generating agents trigger ribosomal impairment and ZAKα activation. Conversely, zebrafish larvae deficient for ZAKα are protected from ROS-induced pathology. Livers of mice fed a ROS-generating diet exhibit ZAKα-activating changes in ribosomal elongation dynamics. Highlighting a role for the RSR in metabolic regulation, ZAK-knockout mice are protected from developing high-fat high-sugar (HFHS) diet-induced blood glucose intolerance and liver steatosis. Finally, ZAK ablation slows animals from developing the hallmarks of metabolic aging. Our work highlights ROS-induced ribosomal impairment as a physiological activation signal for ZAKα that underlies metabolic adaptation in obesity and aging.
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