PUBLICATION

Midkine-a functions as a universal regulator of proliferation during epimorphic regeneration in adult zebrafish

Authors
Ang, N.B., Saera-Vila, A., Walsh, C., Hitchcock, P.F., Kahana, A., Thummel, R., Nagashima, M.
ID
ZDB-PUB-200613-11
Date
2020
Source
PLoS One   15: e0232308 (Journal)
Registered Authors
Hitchcock, Peter, Kahana, Alon, Nagashima, Mikiko, Thummel, Ryan
Keywords
none
MeSH Terms
  • Animal Fins/physiology
  • Animals
  • Animals, Genetically Modified/metabolism
  • Cell Differentiation
  • Cell Proliferation
  • Midkine/genetics
  • Midkine/metabolism*
  • Mutagenesis
  • Neuroglia/cytology
  • Neuroglia/metabolism
  • Oculomotor Muscles/physiology
  • Regeneration/physiology*
  • Retinal Neurons/physiology
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
32530962 Full text @ PLoS One
Abstract
Zebrafish have the ability to regenerate damaged cells and tissues by activating quiescent stem and progenitor cells or reprogramming differentiated cells into regeneration-competent precursors. Proliferation among the cells that will functionally restore injured tissues is a fundamental biological process underlying regeneration. Midkine-a is a cytokine growth factor, whose expression is strongly induced by injury in a variety of tissues across a range of vertebrate classes. Using a zebrafish Midkine-a loss of function mutant, we evaluated regeneration of caudal fin, extraocular muscle and retinal neurons to investigate the function of Midkine-a during epimorphic regeneration. In wildtype zebrafish, injury among these tissues induces robust proliferation and rapid regeneration. In Midkine-a mutants, the initial proliferation in each of these tissues is significantly diminished or absent. Regeneration of the caudal fin and extraocular muscle is delayed; regeneration of the retina is nearly completely absent. These data demonstrate that Midkine-a is universally required in the signaling pathways that convert tissue injury into the initial burst of cell proliferation. Further, these data highlight differences in the molecular mechanisms that regulate epimorphic regeneration in zebrafish.
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Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
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Mapping