Present addresses Department of Oral Biology, School of Dentistry, University of Oslo, Oslo, Norway; †Shanghai Research Center for Biomodel Organism, China.
Regional regulation of palatal growth and patterning along the anterior–posterior axis in mice
Version of Record online: 2 NOV 2005
Journal of Anatomy
Volume 207, Issue 5, pages 655–667, November 2005
How to Cite
Hilliard, S. A., Yu, L., Gu, S., Zhang, Z. and Chen, Y. P. (2005), Regional regulation of palatal growth and patterning along the anterior–posterior axis in mice. Journal of Anatomy, 207: 655–667. doi: 10.1111/j.1469-7580.2005.00474.x
- Issue online: 2 NOV 2005
- Version of Record online: 2 NOV 2005
- Accepted for publication 20 July 2005
- cleft palate;
- epithelial–mesenchymal interaction;
- growth factor;
- transcription factor
Cleft palate is a congenital disorder arising from a failure in the multistep process of palate development. In its mildest form the cleft affects only the posterior soft palate. In more severe cases the cleft includes the soft (posterior) and hard (anterior) palate. In mice a number of genes show differential expression along the anterior–posterior axis of the palate. Mesenchymal heterogeneity is established early, as evident from Bmp4-mediated induction of Msx1 and cell proliferation exclusively in the anterior and Fgf8-specific induction of Pax9 in the posterior palate alone. In addition, the anterior palatal epithelium has the unique ability to induce Shox2 expression in the anterior mesenchyme in vivo and the posterior mesenchyme in vitro. Therefore, the induction and competence potentials of the epithelium and mesenchyme in the anterior are clearly distinct from those in the posterior. Defective growth in the anterior palate of Msx1−/– and Fgf10−/– mice leads to a complete cleft palate and supports the anterior-to-posterior direction of palatal closure. By contrast, the Shox2−/– mice exhibit incomplete clefts in the anterior presumptive hard palate with an intact posterior palate. This phenotype cannot be explained by the prevailing model of palatal closure. The ability of the posterior palate to fuse independent of the anterior palate in Shox2−/– mice underscores the intrinsic differences along the anterior–posterior axis of the palate. We must hitherto consider the heterogeneity of gene expression and function in the palate to understand better the aetiology and pathogenesis of non-syndromic cleft palate and the mechanics of normal palatogenesis.