Abnormal lens morphogenesis and ectopic lens formation in the absence of beta-catenin function
Language English Country United States Media print
Document type Journal Article
PubMed
17410548
DOI
10.1002/dvg.20277
Knihovny.cz E-resources
- MeSH
- beta Catenin genetics physiology MeSH
- Cell Adhesion MeSH
- Choristoma congenital genetics MeSH
- Morphogenesis genetics MeSH
- Mice, Transgenic MeSH
- Mice MeSH
- Nose Diseases congenital genetics MeSH
- Eye embryology MeSH
- Lens, Crystalline cytology embryology MeSH
- Wnt Proteins physiology MeSH
- Signal Transduction genetics MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- beta Catenin MeSH
- Wnt Proteins MeSH
beta-Catenin plays a key role in cadherin-mediated cell adhesion as well as in canonical Wnt signaling. To study the role of beta-catenin during eye development, we used conditional Cre/loxP system in mouse to inactivate beta-catenin in developing lens and retina. Inactivation of beta-catenin does not suppress lens fate, but instead results in abnormal morphogenesis of the lens. Using BAT-gal reporter mice, we show that beta-catenin-mediated Wnt signaling is notably absent from lens and neuroretina throughout eye development. The observed defect is therefore likely due to the cytoskeletal role of beta-catenin, and is accompanied by impaired epithelial cell adhesion. In contrast, inactivation of beta-catenin in the nasal ectoderm, an area with active Wnt signaling, results in formation of crystallin-positive ectopic lentoid bodies. These data suggest that, outside of the normal lens, beta-catenin functions as a coactivator of canonical Wnt signaling to suppress lens fate.
References provided by Crossref.org
WNT/β-Catenin Signaling in Vertebrate Eye Development
Non-essential role for cilia in coordinating precise alignment of lens fibres