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Lifespan extension induced by AMPK and calcineurin is mediated by CRTC-1 and CREB

Author

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  • William Mair

    (The Salk Institute for Biological Studies
    Howard Hughes Medical Institute, The Salk Institute for Biological Studies
    The Glenn Foundation for Medical Research, The Salk Institute for Biological Studies)

  • Ianessa Morantte

    (The Salk Institute for Biological Studies
    Howard Hughes Medical Institute, The Salk Institute for Biological Studies
    The Glenn Foundation for Medical Research, The Salk Institute for Biological Studies)

  • Ana P. C. Rodrigues

    (The Salk Institute for Biological Studies
    Razavi Newman Center for Bioinformatics, The Salk Institute for Biological Studies)

  • Gerard Manning

    (The Salk Institute for Biological Studies
    Razavi Newman Center for Bioinformatics, The Salk Institute for Biological Studies)

  • Marc Montminy

    (The Salk Institute for Biological Studies
    The Glenn Foundation for Medical Research, The Salk Institute for Biological Studies)

  • Reuben J. Shaw

    (The Salk Institute for Biological Studies
    Howard Hughes Medical Institute, The Salk Institute for Biological Studies
    The Glenn Foundation for Medical Research, The Salk Institute for Biological Studies)

  • Andrew Dillin

    (The Salk Institute for Biological Studies
    Howard Hughes Medical Institute, The Salk Institute for Biological Studies
    The Glenn Foundation for Medical Research, The Salk Institute for Biological Studies)

Abstract

CTRCs as ageing mediators Ageing is slowed, and lifespan extended, in the nematode Caenorhabditis elegans by the activation of the enzyme AMPK (5′ adenosine monophosphate-activated protein kinase) or by inactivation of the protein phosphatase calcineurin. The nature of the related molecular pathways involved has remained unclear, but here it is shown that inhibition of CRTC-1, the sole CREB-regulated transcriptional activator in C. elegans, is required for these life-extending effects. Eliminating the crtc-1 gene increases lifespan in a crh-1 dependent manner, as does elimination of crh-1 (the gene for CREB homologue 1) alone. Downregulation of components in the CRTC/CREB pathway has been shown to confer health benefits to mice, complementing their lifespan effects in worms, and it will be interesting to discover whether CTRCs act as ageing modulators more generally in mammals.

Suggested Citation

  • William Mair & Ianessa Morantte & Ana P. C. Rodrigues & Gerard Manning & Marc Montminy & Reuben J. Shaw & Andrew Dillin, 2011. "Lifespan extension induced by AMPK and calcineurin is mediated by CRTC-1 and CREB," Nature, Nature, vol. 470(7334), pages 404-408, February.
    • Handle: RePEc:nat:nature:v:470:y:2011:i:7334:d:10.1038_nature09706
    DOI: 10.1038/nature09706
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    Cited by:

    1. Elite Possik & Laura-Lee Klein & Perla Sanjab & Ruyuan Zhu & Laurence Côté & Ying Bai & Dongwei Zhang & Howard Sun & Anfal Al-Mass & Abel Oppong & Rasheed Ahmad & Alex Parker & S.R. Murthy Madiraju & , 2023. "Glycerol 3-phosphate phosphatase/PGPH-2 counters metabolic stress and promotes healthy aging via a glycogen sensing-AMPK-HLH-30-autophagy axis in C. elegans," Nature Communications, Nature, vol. 14(1), pages 1-18, December.

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