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Abnormal lens morphogenesis and ectopic lens formation in the absence of β‐catenin function
Author(s) -
Kreslova Jana,
Machon Ondrej,
Ruzickova Jana,
Lachova Jitka,
Wawrousek Eric F.,
Kemler Rolf,
Krauss Stefan,
Piatigorsky Joram,
Kozmik Zbynek
Publication year - 2007
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20277
Subject(s) - wnt signaling pathway , microbiology and biotechnology , morphogenesis , ectopic expression , biology , lens (geology) , catenin , beta catenin , cell fate determination , ectoderm , cell adhesion , eye development , signal transduction , cadherin , cell , phenotype , embryogenesis , genetics , cell culture , transcription factor , embryo , paleontology , gene
Abstract 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. genesis 45:157–168, 2007. Published 2007 Wiley‐Liss, Inc.