Disruption of the palatal rugae pattern in Tabby (eda) mutant mice

Eur J Oral Sci. 2007 Dec;115(6):441-8. doi: 10.1111/j.1600-0722.2007.00482.x.

Abstract

The eda mouse gene is linked with anomalies of ectodermal derivatives, such as hair, glands, and teeth. The palatal rugae (oral mucosa foldings on the hard palate) are also ectodermal derivatives. Therefore, we searched for and compared palatal rugae anomalies of Tabby mice bearing a mutation in the eda gene with their wild-type counterparts. We compared the number and shape of palatal rugae in 179 mutant and 102 wild-type mice from four different stocks of Tabby mice. Palatal rugae anomalies were documented at a low frequency in wild-type mice of different backgrounds, which may reflect a lack of robustness of palatal rugae development. However, the proportion of anomalies observed in the C57BL/6J background makes us recommend avoiding its use in further palate studies. We showed statistically that the phenotypic variability seen in wild-type animals is further increased in Tabby mutants. The anomalies mainly included various forms of reduction, with rugae IV-VI being more frequently affected. Those rugae were shortened, dotted or absent (mainly ruga V). By analogy to the role played by eda in other ectodermal derivatives, we propose that it might play a role in defining the pattern of the palatal rugae.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alleles
  • Animals
  • Ectodysplasins / genetics*
  • Edar Receptor / genetics
  • Female
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Palate, Hard / abnormalities*
  • Phenotype
  • Sex Factors

Substances

  • Ectodysplasins
  • Eda protein, mouse
  • Edar Receptor
  • Edar protein, mouse