PUBLICATION

Mutations in N-cadherin and a Stardust homolog, Nagie oko, affect cell-cycle exit in zebrafish retina

Authors
Yamaguchi, M., Imai, F., Tonou-Fujimori, N., and Masai, I.
ID
ZDB-PUB-100408-18
Date
2010
Source
Mechanisms of Development   127(5-6): 247-264 (Journal)
Registered Authors
Imai, Fumiyasu, Masai, Ichiro, Yamaguchi, Masahiro
Keywords
Cell polarity, Adherens junction, Cell division, Neurogenesis, Retina, Zebrafish, Notch, PKA, N-cadherin, Nagie oko
MeSH Terms
  • Cell Cycle/genetics*
  • Signal Transduction/genetics
  • In Situ Hybridization
  • Retina/cytology*
  • Retina/metabolism
  • Mutation
  • Animals, Genetically Modified
  • Cadherins/genetics*
  • Cadherins/metabolism
  • Guanylate Cyclase/genetics*
  • Guanylate Cyclase/metabolism
  • Receptors, Notch/genetics
  • Receptors, Notch/metabolism
  • Adherens Junctions/genetics
  • Adherens Junctions/metabolism
  • Stem Cells/cytology
  • Stem Cells/metabolism
  • Cell Polarity/genetics
  • Zebrafish/genetics*
  • Zebrafish/metabolism
  • Apoptosis/genetics
  • Gene Expression Regulation, Developmental
  • Cell Count
  • Zebrafish Proteins/genetics*
  • Zebrafish Proteins/metabolism
  • Fluorescent Antibody Technique
  • Cell Proliferation
  • Cell Differentiation/genetics
  • Animals
(all 29)
PubMed
20362667 Full text @ Mech. Dev.
Abstract
It has been reported that the loss of apicobasal cell polarity and the disruption of adherens junctions induce hyperplasia in the mouse developing brain. However, it is not fully understood whether hyperplasia is caused by an enhanced cell proliferation, an inhibited neurogenesis, or both. In this study, we found that the ratio of the number of proliferating progenitor cells to the total number of retinal cells increases in the neurogenic stages in zebrafish n-cadherin (ncad) and nagie oko (nok) mutants, in which the apicobasal cell polarity and adherens junctions in the retinal epithelium are disrupted. The cell-cycle progression was not altered in the ncad and nok mutants. Rather, the ratio of the number of cells undergoing neurogenic cell division to the total number of cells undergoing mitosis decreased in the ncad and nok mutant retinas, suggesting that the switching from proliferative cell division to neurogenic cell division was compromised in these mutant retinas. These findings suggest that the inhibition of neurogenesis is a primary defect that causes hyperplasia in the ncad and nok mutant retinas. The Hedgehog-protein kinase A signaling pathway and the Notch signaling pathway regulate retinal neurogenesis in zebrafish. We found that both signaling pathways are involved in the generation of neurogenic defects in the ncad and nok mutant retinas. Taken together, these findings suggest that apicobasal cell polarity and epithelial integrity are essential for retinal neurogenesis in zebrafish.
Genes / Markers
Figures
Figure Gallery (7 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b577
    Point Mutation
    fr7
      Point Mutation
      rw021TgTransgenic Insertion
        rw161
          Unknown
          rw170
            Unknown
            rw267
              Unknown
              rw310
                Unknown
                rw399
                  Point Mutation
                  rw407
                    Unknown
                    rw464
                      Unknown
                      1 - 10 of 12
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                      Human Disease / Model
                      No data available
                      Sequence Targeting Reagents
                      No data available
                      Fish
                      Antibodies
                      No data available
                      Orthology
                      No data available
                      Engineered Foreign Genes
                      Marker Marker Type Name
                      GFPEFGGFP
                      1 - 1 of 1
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                      Mapping
                      No data available