PUBLICATION

N-cadherin regulates primary motor axon growth and branching during zebrafish embryonic development

Authors
Bruses, J.L.
ID
ZDB-PUB-110502-7
Date
2011
Source
The Journal of comparative neurology   519(9): 1797-1815 (Journal)
Registered Authors
Bruses, Juan L.
Keywords
cell adhesion molecules, N-cadherin, zebrafish development, primary motor neurons, axonal pathfinding, neuromuscular junction
MeSH Terms
  • Gene Targeting
  • Cell Differentiation/genetics
  • Cell Differentiation/physiology
  • Zebrafish Proteins/deficiency
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
  • Cricetulus
  • Neurogenesis/genetics
  • Neurogenesis/physiology*
  • Zebrafish
  • Axons/physiology*
  • Body Patterning/genetics
  • Body Patterning/physiology
  • CHO Cells
  • Spinal Cord/cytology
  • Spinal Cord/embryology
  • Animals
  • Motor Neurons/cytology
  • Motor Neurons/physiology*
  • Cricetinae
  • Cadherins/deficiency
  • Cadherins/genetics
  • Cadherins/physiology*
  • Mutation/physiology
(all 24)
PubMed
21452216 Full text @ J. Comp. Neurol.
Abstract
N-cadherin is a classical type I cadherin that contributes to the formation of neural circuits by regulating growth cone migration and the formation of synaptic contacts. This study analyzed the role of N-cadherin in primary motor axons growth during development of the zebrafish (Danio rerio) embryo. After exiting the spinal cord, primary motor axons migrate ventrally through a common pathway and form the first neuromuscular junction with the muscle pioneer cells located at the horizontal myoseptum, which serves as a choice point for cell-type-specific pathway selection. Analysis of N-cadherin mutants (cdh2hi3644Tg) and embryos injected with N-cadherin antisense morpholinos showed primary motor axons extending aberrant axonal branches at the choice point in <40% of the somitic hemisegments and an <150% increase in the number of branches per axon length within the ventral myotome. Analysis of individual axons trajectories showed that the caudal (CaP) and rostral (RoP) motor neurons axons formed aberrant branches at the choice point that abnormally extended in the rostrocaudal axis and ventrally to the horizontal myoseptum. Expression of a dominant-interfering N-cadherin cytoplasmic domain in primary motor neurons caused some axons to stall abnormally at the horizontal myoseptum and to impair their migration into the ventral myotome. However, in N-cadherin-depleted embryos, the majority of primary motor axons innervated their appropriate myotomal territories, indicating that N-cadherin regulates motor axon growth and branching without severely affecting the mechanisms that control axonal target selection.
Genes / Markers
Figures
Figure Gallery (8 images)
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Expression
No data available
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
hi3644TgTransgenic Insertion
ml2TgTransgenic Insertion
    s300tTgTransgenic Insertion
      1 - 3 of 3
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      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      cdh2MO1-cdh2MRPHLNO
      1 - 1 of 1
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      Fish
      Antibodies
      Name Type Antigen Genes Isotypes Host Organism
      Ab-SV2monoclonal
        IgG1Mouse
        znp-1monoclonalIgG2aMouse
        1 - 2 of 2
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        Orthology
        No data available
        Engineered Foreign Genes
        Marker Marker Type Name
        GAL4EFGGAL4
        GFPEFGGFP
        1 - 2 of 2
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        Mapping
        No data available