Drp1-mediated mitochondrial fission regulates calcium and F-actin dynamics during wound healing

Susana Ponte, Lara Carvalho, Maria Gagliardi, Isabel Campos, Paulo J Oliveira, António Jacinto

Research output: Contribution to journalArticlepeer-review

21 Citations (Scopus)
58 Downloads (Pure)


Mitochondria adapt to cellular needs by changes in morphology through fusion and fission events, referred to as mitochondrial dynamics. Mitochondrial function and morphology are intimately connected and the dysregulation of mitochondrial dynamics is linked to several human diseases. In this work, we investigated the role of mitochondrial dynamics in wound healing in the Drosophila embryonic epidermis. Mutants for mitochondrial fusion and fission proteins fail to close their wounds, indicating that the regulation of mitochondrial dynamics is required for wound healing. By live-imaging, we found that loss of function of the mitochondrial fission protein Dynamin-related protein 1 (Drp1) compromises the increase of cytosolic and mitochondrial calcium upon wounding and leads to reduced ROS production and F-actin defects at the wound edge, culminating in wound healing impairment. Our results highlight a new role for mitochondrial dynamics in the regulation of calcium, ROS and F-actin during epithelial repair.

Original languageEnglish
Article numberbio048629
Issue number5
Early online date17 Mar 2020
Publication statusPublished - May 2020


  • Calcium
  • Drp1
  • F-actin
  • Mitochondria
  • Mitochondrial dynamics
  • Wound healing


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