MSX1 DEFICIENT MICE EXHIBIT CLEFT-PALATE AND ABNORMALITIES OF CRANIOFACIAL AND TOOTH DEVELOPMENT

The Msx1 homeobox gene is expressed at diverse sites of epithelial-mes enchymal interaction during vertebrate embryogenesis, and has been imp licated in signalling processes between tissue layers. To determine th e phenotypic consequences of its deficiency, we prepared mice lacking Msx1 function. All Msx1-homczygotes manifest a cleft secondary palate, a deficiency of alveolar mandible and maxilla and a failure of tooth development. These mice also exhibit abnormalities of the nasal, front al and parietal bones, and of the malleus in the middle ear. Msx1 thus has a critical role in mediating epithelial-mesenchymal interactions during craniofacial bone and tooth development. The Msx1-/Msx1- phenot ype is similar to human cleft palate, and provides a genetic model for cleft palate and oligodontia in which the defective gene is known.