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• W26657511 abstract "Craniofacial malformations such as oral clefts anddental abnormalities are common congenital diseases, which arisefrom the disruption of various steps of normal craniofacialdevelopment. Previous studies have established important roles ofseveral core signaling pathways, including Shh, Bmp and Fgfsignaling, in secondary palate and early tooth development.However, very little is known about the role of canonical Wntsignaling in palatogenesis. Moreover, whereas canonical Wntsignaling has been shown to play critical roles in the developingdental epithelium, whether it is also required in the toothmesenchyme for activation of the odontogenic potential is notknown. In this thesis, I showed that canonical Wnt signaling wasnot activated in most palatal mesenchymal cells by analysis ofcanonical Wnt signaling reporter mice. To test the requirement ofinactivation/inhibition of canonical Wnt signaling in normalpalatogenesis, I utilized the Cre/Lox system to conditionallystabilize β-catein in palatal mesenchymal cells. Persistentactivation of canonical Wnt signaling in palatal mesenchymal cellsled to cleft palate. Detailed histological analysis indicated thatelevation of palatal shelves did not occur in the β-cateningain-of-function mutants. To investigate the cellular mechanismsunderlying the cleft palate phenotype, I performed BrdU labelingand TUNEL assays to detect alterations in cell proliferation andcell death, and found that cell proliferation was reduced in bothpalatal epithelium and mesenchyme in mutants compared to those ofcontrol littermates at E13.5, while cell death was similar incontrol and mutant littermates. To investigate which downstreamgene(s)/pathway(s) were affected, I analyzed the expression ofgenes important for secondary palate development by in-situhybridization, and revealed that the expression of Lef1, Bmp4,Bmp2, and Osr2 was increased, while the expression of Shox2 wastotally abolished in palatal mesenchyme of mutant embryos. Inconclusion, our data indicate canonical Wnt signaling is activelyinhibited in palatal mesenchymal cells during normal palatogenesis.I also investigated the role of mesenchymal Wnt/β-catenin in earlytooth development. I found that tissue-specific inactivation ofβ-catenin, a central component of the canonical Wnt signalingpathway, in the developing early tooth mesenchyme, caused toothdevelopmental arrest at the bud stage in mice. I further showedthat mesenchymal β-catenin function was required for expression ofLef1 and Fgf3 in the developing tooth mesenchyme and for inductionof primary enamel knot in the developing tooth epithelium.Moreover, I found that constitutive stabilization of β-catenin inthe developing palatal mesenchyme induced ectopic tooth initiationfrom the palatal epithelium. Together, these results revealed thatWnt ligands expressed in the presumptive dental epithelium signaldirectly to the developing tooth mesenchyme to activate mesenchymalodontogenic program during tooth initiation." @default.
• W26657511 created "2016-06-24" @default.
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• W26657511 date "2009-01-01" @default.
• W26657511 modified "2023-09-27" @default.
• W26657511 title "Investigating the roles of Wnt/beta-catenin signaling in craniofacial development" @default.
• W26657511 hasPublicationYear "2009" @default.
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