Msx1 deficient mice exhibit cleft palate and abnormalities of craniofacial and tooth development View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1994-04

AUTHORS

I Satokata, R Maas

ABSTRACT

The Msx1 homeobox gene is expressed at diverse sites of epithelial-mesenchymal interaction during vertebrate embryogenesis, and has been implicated in signalling processes between tissue layers. To determine the phenotypic consequences of its deficiency, we prepared mice lacking Msx1 function. All Msx1- homozygotes 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, frontal 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- phenotype is similar to human cleft palate, and provides a genetic model for cleft palate and oligodontia in which the defective gene is known. More... »

PAGES

348-356

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng0494-348

DOI

http://dx.doi.org/10.1038/ng0494-348

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053612890

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/7914451


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