Mice and humans form one or two sets of teeth, respectively, but mutations in the adenomatous polyposis coli (Apc) gene triggers additional tooth formation in both species. Apc encodes a negative regulator of Wnt signalling, and studies in embryonic mice have shown previously that activating Wnt signalling also induces additional teeth. On , Richard Maas and colleagues now reveal that deleting Apc in the oral epithelium of adult mice has a similar effect. Using several transgenic mouse lines, the authors show that without Apc, many different embryonic and juvenile jaw areas generate extra teeth. Additional teeth also form in adult mice, mainly in the incisor region, which contains dental epithelial stem cells. The effects of Apc deficiency are non-cell-autonomous and mediated byβ-catenin, with Fgf8, an early tooth initiation marker, being one target of Wnt/β-catenin signalling. Surprisingly, extra teeth can form in the absence of the homeobox gene Msx1, which is required for normal tooth formation. Future studies could see the application of these findings to tooth repair and regeneration in humans.
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