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Insulin and TOR signal in parallel through FOXO and S6K to promote epithelial wound healing

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  • Parisa Kakanj

    (Institute for Genetics, University of Cologne
    Max Planck Institute for Biology of Ageing
    Center for Molecular Medicine Cologne, University of Cologne)

  • Bernard Moussian

    (Institute of Biology Valrose (IBV), University of Nice-Sophia Antipolis)

  • Sebastian Grönke

    (Max Planck Institute for Biology of Ageing)

  • Victor Bustos

    (Max Planck Institute for Biology of Ageing)

  • Sabine A. Eming

    (Center for Molecular Medicine Cologne, University of Cologne
    University of Cologne
    Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne)

  • Linda Partridge

    (Max Planck Institute for Biology of Ageing
    Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne
    Institute of Healthy Ageing, Evolution, and Environment, University College London)

  • Maria Leptin

    (Institute for Genetics, University of Cologne
    Center for Molecular Medicine Cologne, University of Cologne
    European Molecular Biology Laboratory)

Abstract

The TOR and Insulin/IGF signalling (IIS) network controls growth, metabolism and ageing. Although reducing TOR or insulin signalling can be beneficial for ageing, it can be detrimental for wound healing, but the reasons for this difference are unknown. Here we show that IIS is activated in the cells surrounding an epidermal wound in Drosophila melanogaster larvae, resulting in PI3K activation and redistribution of the transcription factor FOXO. Insulin and TOR signalling are independently necessary for normal wound healing, with FOXO and S6K as their respective effectors. IIS is specifically required in cells surrounding the wound, and the effect is independent of glycogen metabolism. Insulin signalling is needed for the efficient assembly of an actomyosin cable around the wound, and constitutively active myosin II regulatory light chain suppresses the effects of reduced IIS. These findings may have implications for the role of insulin signalling and FOXO activation in diabetic wound healing.

Suggested Citation

  • Parisa Kakanj & Bernard Moussian & Sebastian Grönke & Victor Bustos & Sabine A. Eming & Linda Partridge & Maria Leptin, 2016. "Insulin and TOR signal in parallel through FOXO and S6K to promote epithelial wound healing," Nature Communications, Nature, vol. 7(1), pages 1-16, December.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12972
    DOI: 10.1038/ncomms12972
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