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Abnormal Lens Morphogenesis and Ectopic Lens Formation in the Absence of β-Cateinin Function

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Kemler,  Rolf
Emeritus Group: Molecular Embryology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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引用

Kreslova, J., Machon, O., Ruzickova, J., Lachova, J., Wawrousek, E. F., Kemler, R., Krauss, S., Piatigorsky, J., & Kozmik, Z. (2007). Abnormal Lens Morphogenesis and Ectopic Lens Formation in the Absence of β-Cateinin Function. Genesis, 45, 157-168.


引用: https://hdl.handle.net/11858/00-001M-0000-002B-91C7-1
要旨
β-Catenin plays a key role in cadherin-mediated cell adhesion as well as in canonical Wnt signaling. To study the role of β-catenin during eye development, we used conditional Cre/loxP system in mouse to inactivate β-catenin in developing lens and retina. Inactivation of β-catenin does not suppress lens fate, but instead results in abnormal morphogenesis of the lens. Using BAT-gal reporter mice, we show that β-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 β-catenin, and is accompanied by impaired epithelial cell adhesion. In contrast, inactivation of β-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, β-catenin functions as a coactivator of canonical Wnt signaling to suppress lens fate.