PUBLICATION

Bone Regenerates via Dedifferentiation of Osteoblasts in the Zebrafish Fin

Authors
Knopf, F., Hammond, C., Chekuru, A., Kurth, T., Hans, S., Weber, C.W., Mahatma, G., Fisher, S., Brand, M., Schulte-Merker, S., and Weidinger, G.
ID
ZDB-PUB-110524-34
Date
2011
Source
Developmental Cell   20(5): 713-724 (Journal)
Registered Authors
Brand, Michael, Chekuru, Avinash, Fisher, Shannon, Hammond, Chrissy, Hans, Stefan, Knopf, Franziska, Schulte-Merker, Stefan, Weidinger, Gilbert
Keywords
none
MeSH Terms
  • Animal Fins/cytology
  • Animal Fins/metabolism*
  • Animals
  • Bone and Bones/cytology
  • Bone and Bones/metabolism*
  • Cell Dedifferentiation
  • Down-Regulation
  • Osteoblasts/cytology
  • Osteoblasts/metabolism*
  • Zebrafish
PubMed
21571227 Full text @ Dev. Cell
Abstract
While mammals have a limited capacity to repair bone defects, zebrafish can completely regenerate amputated bony structures of their fins. Fin regeneration is dependent on formation of a blastema, a progenitor cell pool accumulating at the amputation plane. It is unclear which cells the blastema is derived from, whether it forms by dedifferentiation of mature cells, and whether blastema cells are multipotent. We show that mature osteoblasts dedifferentiate and form part of the blastema. Osteoblasts downregulate expression of intermediate and late bone differentiation markers and induce genes expressed by bone progenitors. Dedifferentiated osteoblasts proliferate in a FGF-dependent manner and migrate to form part of the blastema. Genetic fate mapping shows that osteoblasts only give rise to osteoblasts in the regenerate, indicating that dedifferentiation is not associated with the attainment of multipotency. Thus, bone can regenerate from mature osteoblasts via dedifferentiation, a finding with potential implications for human bone repair.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping