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Publication : Disruption of eyelid and cornea morphogenesis by epithelial β-catenin gain-of-function.

First Author  Mizoguchi S Year  2015
Journal  Mol Vis Volume  21
Pages  793-803 PubMed ID  26283861
Mgi Jnum  J:226707 Mgi Id  MGI:5698307
Citation  Mizoguchi S, et al. (2015) Disruption of eyelid and cornea morphogenesis by epithelial beta-catenin gain-of-function. Mol Vis 21:793-803
abstractText  PURPOSE: To examine the developmental pathobiology of the eyelid and the cornea caused by epithelial beta-catenin gain-of-function (gof) during mouse embryogenesis. METHODS: Compound mutant mice (Ctnnb1(GOFOSE) , gof of beta-catenin in the epidermis and the ocular surface epithelium) were generated by time-mating keratin 5-promoter-Cre recombinase (Krt5-Cre) and Ctnnb1(fE3/WT) (floxed exon 3 of Ctnnb1) mice. Eyes obtained from wild-type (WT) and mutant embryos at various gestation stages until E18.5 were examined with histology and immunohistochemistry. The ultrastructure of the ocular tissues of the E18.5 embryos was also examined. RESULTS: Expression of the gof-beta-catenin mutant protein in the epidermis severely impaired eyelid morphogenesis at E15.5, E17.5, and E18.5. The mutant stroma exhibited impaired keratocyte differentiation with accelerated cell proliferation and reduction in the accumulation of collagen type I. The mutant embryos also showed hyperproliferative nodules in the ocular surface epithelia with anomaly of cornea-type epithelial differentiation and the absence of the epithelial basement membrane. CONCLUSIONS: Expression of the gof-beta-catenin mutant protein in basal epithelial cells disrupts eyelid and cornea morphogenesis during mouse embryonic development due to the perturbation of cell proliferation and differentiation of the epithelium and the neural crest-derived mesenchyme.
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