Similar to the biology of hair follicles, K14-cre–driven loss of Apc also affected the development of other epidermal appendages that depend on epithelial–mesenchymal interactions for their formation. The most striking of these was dental dysplasia (Figure 4K–4R). Tooth development is normally initiated between E11 and E12 by invagination of ectodermally derived oral epithelium into the underlying cranial neural crest–derived mesenchyme, generating a tooth germ. Despite the grossly toothless phenotype of KA mutants, histological analysis of their oral cavities revealed the formation of multiple tooth buds at each location. These aberrant teeth obviously failed to grow out during the dietary transition from milk to solid food. Analogous to the expression patterns of K14 and β-catenin in the normal skin, diffuse membrane-bound expression of β-catenin was detected in K14-expressing oral epithelium and ameloblasts of normal mice. In mutants, some of the K14-expressing cells also showed strong cytosolic/nuclear β-catenin staining, as observed in the mutant skin (Figure 4Q, 4Q′, and 4R). Initiation of ectopic tooth buds in the mutant mice was evident at E15.5 by extra dots of Shh expression adjacent to the primary teeth (data not shown).