ZFIN ID: ZDB-PUB-121016-21
Early redox, Src family kinase, and calcium signaling integrate wound responses and tissue regeneration in zebrafish
Yoo, S.K., Freisinger, C.M., Lebert, D.C., and Huttenlocher, A.
Date: 2012
Source: The Journal of cell biology   199(2): 225-234 (Journal)
Registered Authors: Huttenlocher, Anna
Keywords: none
MeSH Terms:
  • Animal Fins/injuries
  • Animal Fins/metabolism
  • Animals
  • Calcium Signaling*
  • Hydrogen Peroxide/metabolism
  • Oxidation-Reduction
  • Proto-Oncogene Proteins c-fyn/genetics
  • Proto-Oncogene Proteins c-fyn/metabolism
  • Proto-Oncogene Proteins c-yes/genetics
  • Proto-Oncogene Proteins c-yes/metabolism
  • Regeneration/physiology*
  • Wound Healing/physiology*
  • Xenopus Proteins/genetics
  • Xenopus Proteins/metabolism
  • Zebrafish
  • Zebrafish Proteins/metabolism
  • src-Family Kinases/metabolism*
PubMed: 23045550 Full text @ J. Cell Biol.

Tissue injury can lead to scar formation or tissue regeneration. How regenerative animals sense initial tissue injury and transform wound signals into regenerative growth is an unresolved question. Previously, we found that the Src family kinase (SFK) Lyn functions as a redox sensor in leukocytes that detects H2O2 at wounds in zebrafish larvae. In this paper, using zebrafish larval tail fins as a model, we find that wounding rapidly activated SFK and calcium signaling in epithelia. The immediate SFK and calcium signaling in epithelia was important for late epimorphic regeneration of amputated fins. Wound-induced activation of SFKs in epithelia was dependent on injury-generated H2O2. A SFK member, Fynb, was responsible for fin regeneration. This work provides a new link between early wound responses and late regeneration and suggests that redox, SFK, and calcium signaling are immediate “wound signals” that integrate early wound responses and late epimorphic regeneration.