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Saturated very long chain fatty acid configures glycosphingolipid for lysosome homeostasis in long-lived C. elegans

Author

Listed:
  • Feng Wang

    (Chongqing University)

  • Yuxi Dai

    (Chongqing University)

  • Xufeng Zhu

    (ShanghaiTech University)

  • Qilong Chen

    (University of Chinese Academy of Sciences, Chinese Academy of Sciences)

  • Huanhu Zhu

    (ShanghaiTech University)

  • Ben Zhou

    (University of Chinese Academy of Sciences, Chinese Academy of Sciences)

  • Haiqing Tang

    (Chongqing University)

  • Shanshan Pang

    (Chongqing University)

Abstract

The contents of numerous membrane lipids change upon ageing. However, it is unknown whether and how any of these changes are causally linked to lifespan regulation. Acyl chains contribute to the functional specificity of membrane lipids. In this study, working with C. elegans, we identified an acyl chain-specific sphingolipid, C22 glucosylceramide, as a longevity metabolite. Germline deficiency, a conserved lifespan-extending paradigm, induces somatic expression of the fatty acid elongase ELO-3, and behenic acid (22:0) generated by ELO-3 is incorporated into glucosylceramide for lifespan regulation. Mechanistically, C22 glucosylceramide is required for the membrane localization of clathrin, a protein that regulates membrane budding. The reduction in C22 glucosylceramide impairs the clathrin-dependent autophagic lysosome reformation, which subsequently leads to TOR activation and longevity suppression. These findings reveal a mechanistic link between membrane lipids and ageing and suggest a model of lifespan regulation by fatty acid-mediated membrane configuration.

Suggested Citation

  • Feng Wang & Yuxi Dai & Xufeng Zhu & Qilong Chen & Huanhu Zhu & Ben Zhou & Haiqing Tang & Shanshan Pang, 2021. "Saturated very long chain fatty acid configures glycosphingolipid for lysosome homeostasis in long-lived C. elegans," Nature Communications, Nature, vol. 12(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-25398-6
    DOI: 10.1038/s41467-021-25398-6
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