PUBLICATION

N-cadherin mediates retinal lamination, maintenance of forebrain compartments and patterning of retinal neurites

Authors
Masai, I., Lele, Z., Yamaguchi, M., Komori, A., Nakata, A., Nishiwaki, Y., Wada, H., Tanaka, H., Nojima, Y., Hammerschmidt, M., Wilson, S.W., and Okamoto, H.
ID
ZDB-PUB-030602-11
Date
2003
Source
Development (Cambridge, England)   130(11): 2479-2494 (Journal)
Registered Authors
Hammerschmidt, Matthias, Komori, Atsuko, Lele, Zsolt, Masai, Ichiro, Nishiwaki, Yuko, Okamoto, Hitoshi, Tanaka, Hideomi, Wada, Hironori, Wilson, Steve, Yamaguchi, Masahiro
Keywords
none
MeSH Terms
  • Adherens Junctions/metabolism
  • Alleles
  • Animals
  • Base Sequence
  • Body Patterning
  • Cadherins/genetics
  • Cadherins/metabolism*
  • Cell Adhesion
  • Cell Division
  • DNA, Complementary/genetics
  • Mutation
  • Neurons/cytology
  • Prosencephalon/embryology*
  • Prosencephalon/metabolism
  • Receptors, Fibroblast Growth Factor/metabolism
  • Retina/cytology
  • Retina/embryology*
  • Retina/metabolism
  • Retinal Ganglion Cells/cytology
  • Retinal Ganglion Cells/metabolism
  • Signal Transduction
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
12702661 Full text @ Development
Abstract
The complex, yet highly ordered and predictable, structure of the neural retina is one of the most conserved features of the vertebrate central nervous system. In all vertebrate classes, retinal neurons are organized into laminae with each neuronal class adopting specific morphologies and patterns of connectivity. Using genetic analyses in zebrafish, we demonstrate that N-cadherin (Ncad) has several distinct and crucial functions during the establishment of retinal organization. Although the location of cell division is disorganized in embryos with reduced or no Ncad function, different classes of retinal neurons are generated. However, these neurons fail to organize into correct laminae, most probably owing to compromised adhesion between retinal cells. In addition, amacrine cells exhibit exuberant and misdirected outgrowth of neurites that contributes to severe disorganization of the inner plexiform layer. Retinal ganglion cells also exhibit defects in process outgrowth, with axons exhibiting fasciculation defects and adopting incorrect ipsilateral trajectories. At least some of these defects are likely to be due to a failure to maintain compartment boundaries between eye, optic nerve and brain. Although in vitro studies have implicated Fgf receptors in modulating the axon outgrowth promoting properties of Ncad, most aspects of the Ncad mutant phenotype are not phenocopied by treatments that block Fgf receptor function.
Genes / Markers
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes