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
-
- Adherens Junctions/genetics
- Adherens Junctions/metabolism
- Animals
- Animals, Genetically Modified
- Apoptosis/genetics
- Cadherins/genetics*
- Cadherins/metabolism
- Cell Count
- Cell Cycle/genetics*
- Cell Differentiation/genetics
- Cell Polarity/genetics
- Cell Proliferation
- Fluorescent Antibody Technique
- Gene Expression Regulation, Developmental
- Guanylate Cyclase/genetics*
- Guanylate Cyclase/metabolism
- In Situ Hybridization
- Mutation
- Receptors, Notch/genetics
- Receptors, Notch/metabolism
- Retina/cytology*
- Retina/metabolism
- Signal Transduction/genetics
- Stem Cells/cytology
- Stem Cells/metabolism
- Zebrafish/genetics*
- Zebrafish/metabolism
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 20362667 Full text @ Mech. Dev.
Citation
Yamaguchi, M., Imai, F., Tonou-Fujimori, N., and Masai, I. (2010) Mutations in N-cadherin and a Stardust homolog, Nagie oko, affect cell-cycle exit in zebrafish retina. Mechanisms of Development. 127(5-6):247-264.
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
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping