PUBLICATION

Damage-induced reactive oxygen species enable zebrafish tail regeneration by repositioning of Hedgehog expressing cells

Authors
Romero, M.M.G., McCathie, G., Jankun, P., Roehl, H.H.
ID
ZDB-PUB-181003-17
Date
2018
Source
Nature communications   9: 4010 (Journal)
Registered Authors
Roehl, Henry
Keywords
none
MeSH Terms
  • Animals
  • Cell Movement
  • Gene Expression Regulation
  • Hedgehog Proteins/genetics*
  • Hedgehog Proteins/metabolism
  • Models, Biological
  • Notochord/cytology
  • Notochord/metabolism*
  • Reactive Oxygen Species/metabolism*
  • Regeneration*/genetics
  • Signal Transduction/genetics
  • Tail/metabolism
  • Tail/physiology*
  • Wound Healing/genetics
  • Zebrafish/genetics
  • Zebrafish/metabolism
  • Zebrafish/physiology*
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
  • src-Family Kinases/antagonists & inhibitors
PubMed
30275454 Full text @ Nat. Commun.
Abstract
Many aquatic vertebrates have a remarkable ability to regenerate limbs and tails after amputation. Previous studies indicate that reactive oxygen species (ROS) signalling initiates regeneration, but the mechanism by which this takes place is poorly understood. Developmental signalling pathways have been shown to have proregenerative roles in many systems. However, whether these are playing roles that are specific to regeneration, or are simply recapitulating their developmental functions is unclear. Here, we analyse zebrafish larval tail regeneration and find evidence that ROS released upon wounding cause repositioning of notochord cells to the damage site. These cells secrete Hedgehog ligands that are required for regeneration. Hedgehog signalling is not required for normal tail development suggesting that it has a regeneration-specific role. Our results provide a model for how ROS initiate tail regeneration, and indicate that developmental signalling pathways can play regenerative functions that are not directly related to their developmental roles.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping