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

Parisa Kakanj, Bernard Moussian, Sebastian Grönke, Victor Bustos, Sabine A. Eming, Linda Partridge () and Maria Leptin ()
Additional contact information
Parisa Kakanj: Institute for Genetics, 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
Linda Partridge: Max Planck Institute for Biology of Ageing
Maria Leptin: Institute for Genetics, University of Cologne

Nature Communications, 2016, vol. 7, issue 1, 1-16

Abstract: 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.

Date: 2016
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms12972 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms12972

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms12972

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().