The inductive role of Wnt-β-Catenin signaling in the formation of oral apparatus
| Autor: | Takamitsu Maruyama, Genkai J. Huang, Congxing Lin, G. Michael Veith, Liang Ma, Yan Yin, Alexander V. Fisher, Wei Hsu, Maulik Dhandha |
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| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Oral apparatus
medicine.medical_specialty Beta-catenin Primary palate Shh Article Wnt 03 medical and health sciences Mice 0302 clinical medicine Tongue Internal medicine Ectoderm medicine Animals Hedgehog Proteins Molecular Biology beta Catenin 030304 developmental biology Body Patterning Mice Knockout 0303 health sciences Mouth biology Rugae Palate Wnt signaling pathway Mouth Mucosa Gene Expression Regulation Developmental Cell Biology Cell biology Cleft Palate Wnt Proteins Tamoxifen medicine.anatomical_structure Endocrinology Neural Crest Mutation biology.protein Female Hard palate Secondary palate 030217 neurology & neurosurgery Morphogen Developmental Biology Signal Transduction |
| Popis: | Proper patterning and growth of oral structures including teeth, tongue, and palate rely on epithelial–mesenchymal interactions involving coordinated regulation of signal transduction. Understanding molecular mechanisms underpinning oral–facial development will provide novel insights into the etiology of common congenital defects such as cleft palate. In this study, we report that ablating Wnt signaling in the oral epithelium blocks the formation of palatal rugae, which are a set of specialized ectodermal appendages serving as Shh signaling centers during development and niches for sensory cells and possibly neural crest related stem cells in adults. Lack of rugae is also associated with retarded anteroposterior extension of the hard palate and precocious mid-line fusion. These data implicate an obligatory role for canonical Wnt signaling in rugae development. Based on this complex phenotype, we propose that the sequential addition of rugae and its morphogen Shh, is intrinsically coupled to the elongation of the hard palate, and is critical for modulating the growth orientation of palatal shelves. In addition, we observe a unique cleft palate phenotype at the anterior end of the secondary palate, which is likely caused by the severely underdeveloped primary palate in these mutants. Last but not least, we also discover that both Wnt and Shh signalings are essential for tongue development. We provide genetic evidence that disruption of either signaling pathway results in severe microglossia. Altogether, we demonstrate a dynamic role for Wnt-β-Catenin signaling in the development of the oral apparatus. |
| Databáze: | OpenAIRE |
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