Related Experiment Video

Updated: Mar 14, 2026

A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
05:18

A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes

Published on: February 17, 2023

6.1K

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

Parisa Kakanj1,2,3, Bernard Moussian4, Sebastian Grönke2

  • 1Institute for Genetics, University of Cologne, Zülpicherstr. 47a, Cologne 50674, Germany.

Nature Communications
|October 8, 2016
PubMed

Insights

Insulin/IGF signalling (IIS) and TOR pathways are vital for wound healing. IIS activation near wounds promotes healing by enabling actomyosin cable formation, independent of ageing benefits.

Area of Science:

  • Cellular biology
  • Developmental biology
  • Metabolism and aging

Background:

  • The TOR and Insulin/IGF signalling (IIS) network regulates growth, metabolism, and aging.
  • While reduced TOR or insulin signalling benefits aging, its impact on wound healing is detrimental, with underlying reasons unclear.

Purpose of the Study:

  • To investigate the role of IIS and TOR signalling in epidermal wound healing in Drosophila melanogaster larvae.
  • To elucidate the molecular mechanisms by which IIS influences wound repair.

Main Methods:

  • Utilized Drosophila melanogaster larval models to study epidermal wound healing.
  • Investigated the activation of PI3K and redistribution of FOXO transcription factor in response to wounding.
  • Examined the necessity of insulin and TOR signalling pathways and their effectors (FOXO, S6K) for wound repair.
  • Assessed the role of insulin signalling in actomyosin cable assembly and myosin II activity.

Main Results:

  • IIS is activated in cells surrounding epidermal wounds in Drosophila larvae.
  • Both insulin and TOR signalling are independently essential for normal wound healing, with FOXO and S6K as key effectors.
  • IIS is specifically required in the wound-surrounding cells and is independent of glycogen metabolism.
  • Insulin signalling is crucial for the assembly of the actomyosin cable around the wound, and constitutive activation of myosin II suppresses the effects of reduced IIS.

Conclusions:

  • IIS activation in the vicinity of wounds is critical for efficient repair.
  • Insulin signalling directly contributes to wound healing by facilitating actomyosin cable formation.
  • Findings suggest potential implications for understanding diabetic wound healing and the roles of insulin signalling and FOXO activation.

More Related Videos

Murine Excisional Wound Healing Model and Histological Morphometric Wound Analysis06:36

Murine Excisional Wound Healing Model and Histological Morphometric Wound Analysis

Published on: August 21, 2020

14.4K
Adenoviral Gene Therapy for Diabetic Keratopathy: Effects on Wound Healing and Stem Cell Marker Expression in Human Organ-cultured Corneas and Limbal Epithelial Cells11:13

Adenoviral Gene Therapy for Diabetic Keratopathy: Effects on Wound Healing and Stem Cell Marker Expression in Human Organ-cultured Corneas and Limbal Epithelial Cells

Published on: April 7, 2016

9.6K

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.1K
Insulin: The Receptor and Signaling Pathways01:28

Insulin: The Receptor and Signaling Pathways

Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
5.5K
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
2.8K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.6K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
2.6K