PUBLICATION

Dynamics of actinotrichia regeneration in the adult zebrafish fin

Authors
König, D., Page, L., Chassot, B., Jaźwińska, A.
ID
ZDB-PUB-170802-15
Date
2017
Source
Developmental Biology   433(2): 416-432 (Journal)
Registered Authors
Keywords
actinodin, blastema, extracellular matrix, lepidotrichia, osteoblasts, wound epithelium
MeSH Terms
  • Osteoblasts/metabolism
  • Animals
  • Extracellular Matrix/metabolism
  • Regeneration/physiology*
  • Animal Structures/metabolism
  • Animal Structures/ultrastructure
  • Mesoderm
  • Homeostasis
  • Wound Healing/physiology
  • Animal Fins/physiology*
  • Animal Fins/ultrastructure
  • Gene Expression Regulation
  • Zebrafish Proteins/biosynthesis
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
  • Zebrafish/genetics
  • Zebrafish/physiology*
  • Collagen/metabolism
  • Collagen/ultrastructure
(all 19)
PubMed
28760345 Full text @ Dev. Biol.
Abstract
The skeleton of adult zebrafish fins comprises lepidotrichia, which are dermal bones of the rays, and actinotrichia, which are non-mineralized spicules at the distal margin of the appendage. Little is known about the regenerative dynamics of the actinotrichia-specific structural proteins called Actinodins. Here, we used immunofluorescence analysis to determine the contribution of two paralogous Actinodin proteins, And1/2, in regenerating fins. Both proteins were detected in the secretory organelles in the mesenchymal cells of the blastema, but only And1 was detected in the epithelial cells of the wound epithelium. The analysis of whole mount fins throughout the entire regenerative process and longitudinal sections revealed that And1-positive fibers are complementary to the lepidotrichia. The analysis of another longfin fish, a gain-of-function mutation in the potassium channel kcnk5b, revealed that the long-fin phenotype is associated with an extended size of actinotrichia during homeostasis and regeneration. Finally, we investigated the role of several signaling pathways in actinotrichia formation and maintenance. This revealed that the pulse-inhibition of either TGFβ/Activin-βA or FGF are sufficient to impair deposition of Actinodin during regeneration. Thus, the dynamic turnover of Actinodin during fin regeneration is regulated by multiple factors, including the osteoblasts, growth rate in a potassium channel mutant, and instructive signaling networks between the epithelium and the blastema of the regenerating fin.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
pd1TgTransgenic Insertion
    ty86d
      Point Mutation
      zf132TgTransgenic Insertion
        zp3
          Point Mutation
          1 - 4 of 4
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          Human Disease / Model
          No data available
          Sequence Targeting Reagents
          No data available
          Fish
          Antibodies
          Orthology
          No data available
          Engineered Foreign Genes
          Marker Marker Type Name
          EGFPEFGEGFP
          GFPEFGGFP
          1 - 2 of 2
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          Mapping
          No data available