Polyploidization and cell fusion contribute to wound healing in the adult Drosophila epithelium

Curr Biol. 2013 Nov 18;23(22):2224-2232. doi: 10.1016/j.cub.2013.09.029. Epub 2013 Oct 31.

Abstract

Background: Reestablishing epithelial integrity and biosynthetic capacity is critically important following tissue damage. The adult Drosophila abdominal epithelium provides an attractive new system to address how postmitotic diploid cells contribute to repair.

Results: Puncture wounds to the adult Drosophila epidermis close initially by forming a melanized scab. We found that epithelial cells near the wound site fuse to form a giant syncytium, which sends lamellae under the scab to re-epithelialize the damaged site. Other large cells arise more peripherally by initiating endocycles and becoming polyploid, or by cell fusion. Rac GTPase activity is needed for syncytium formation, while the Hippo signaling effector Yorkie modulates both polyploidization and cell fusion. Large cell formation is functionally important because when both polyploidization and fusion are blocked, wounds do not re-epithelialize.

Conclusions: Our observations indicate that cell mass lost upon wounding can be replaced by polyploidization instead of mitotic proliferation. We propose that large cells generated by polyploidization or cell fusion are essential because they are better able than diploid cells to mechanically stabilize wounds, especially those containing permanent acellular structures, such as scar tissue.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abdominal Injuries / pathology
  • Age Factors
  • Animals
  • Animals, Genetically Modified
  • Cell Cycle
  • Cell Fusion*
  • Cyclin E / genetics
  • Cyclin E / metabolism
  • Drosophila / cytology
  • Drosophila / physiology*
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism*
  • Epithelial Cells / metabolism
  • Intracellular Signaling Peptides and Proteins / genetics
  • Intracellular Signaling Peptides and Proteins / metabolism
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Polyploidy*
  • Protein-Serine-Threonine Kinases / genetics
  • Protein-Serine-Threonine Kinases / metabolism
  • Trans-Activators / genetics
  • Trans-Activators / metabolism*
  • Wound Healing / physiology*
  • rac GTP-Binding Proteins / genetics
  • rac GTP-Binding Proteins / metabolism

Substances

  • Cyclin E
  • Drosophila Proteins
  • Intracellular Signaling Peptides and Proteins
  • Nuclear Proteins
  • Trans-Activators
  • Yki protein, Drosophila
  • Protein-Serine-Threonine Kinases
  • hpo protein, Drosophila
  • rac GTP-Binding Proteins