PUBLICATION

Loss of adenomatous polyposis coli (apc) results in an expanded ciliary marginal zone in the zebrafish eye

Authors
Stephens, W.Z., Senecal, M., Nguyen, M., and Piotrowski, T.
ID
ZDB-PUB-100621-23
Date
2010
Source
Developmental Dynamics : an official publication of the American Association of Anatomists   239(7): 2066-2077 (Journal)
Registered Authors
Nguyen, Minh Tu, Piotrowski, Tatjana
Keywords
ciliary marginal zone, Wnt/β-catenin, dkk1, axin2, lef1, retina, sox2, atoh7, follistatin, proliferation, neurogenesis, stem cells, zebrafish, meis1, pax2a, myca, cyclinD1, retinal stem cells
MeSH Terms
  • Adenomatous Polyposis Coli Protein/genetics*
  • Adenomatous Polyposis Coli Protein/metabolism*
  • Animals
  • Eye/embryology*
  • Eye/metabolism*
  • Immunohistochemistry
  • In Situ Hybridization
  • In Situ Nick-End Labeling
  • Signal Transduction
  • Wnt Proteins/metabolism
  • Zebrafish/embryology
  • Zebrafish/metabolism
  • beta Catenin/metabolism
PubMed
20549742 Full text @ Dev. Dyn.
Abstract
The distal region of neural retina (ciliary marginal zone [CMZ]) contains stem cells that produce non-neural and neuronal progenitors. We provide a detailed gene expression analysis of the eyes of apc mutant zebrafish where the Wnt/beta-catenin pathway is constitutively active. Wnt/beta-catenin signaling leads to an expansion of the CMZ accompanied by a central shift of the retinal identity gene sox2 and the proneural gene atoh7. This suggests an important role for peripheral Wnt/beta-catenin signaling in regulating the expression and localization of neurogenic genes in the central retina. Retinal identity genes rx1 and vsx2, as well as meis1 and pax6a act upstream of Wnt/beta-catenin pathway activation. Peripheral cells that likely contain stem cells can be identified by the expression of follistatin, otx1, and axin2 and the lack of expression of myca and cyclinD1. Our results introduce the zebrafish apc mutation as a new model to study signaling pathways regulating the CMZ.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping