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First published online May 8, 2009
doi: 10.1242/10.1242/dev.033803

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Apc inhibition of Wnt signaling regulates supernumerary tooth formation during embryogenesis and throughout adulthood

Xiu-Ping Wang^1,*, Daniel J. O'Connell^1,*, Jennifer J. Lund¹, Irfan Saadi¹, Mari Kuraguchi¹, Annick Turbe-Doan¹, Resy Cavallesco¹, Hyunsoo Kim², Peter J. Park³, Hidemitsu Harada⁴, Raju Kucherlapati^1,5 and Richard L. Maas^1,

¹ Division of Genetics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
² Division of The Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
³ Children's Hospital Informatics Program and Department of Pediatrics, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
⁴ Department of Oral Anatomy, School of Dentistry, Iwate Medical University, Iwate 020-8505, Japan.
⁵ Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.

Author for correspondence (e-mail: maas{at}genetics.med.harvard.edu)

Accepted 31 March 2009

The ablation of Apc function or the constitutive activation of β-catenin in embryonic mouse oral epithelium results in supernumerary tooth formation, but the underlying mechanisms and whether adult tissues retain this potential are unknown. Here we show that supernumerary teeth can form from multiple regions of the jaw and that they are properly mineralized, vascularized, innervated and can start to form roots. Even adult dental tissues can form new teeth in response to either epithelial Apc loss-of-function or β-catenin activation, and the effect of Apc deficiency is mediated by β-catenin. The formation of supernumerary teeth via Apc loss-of-function is non-cell-autonomous. A small number of Apc-deficient cells is sufficient to induce surrounding wild-type epithelial and mesenchymal cells to participate in the formation of new teeth. Strikingly, Msx1, which is necessary for endogenous tooth development, is dispensable for supernumerary tooth formation. In addition, we identify Fgf8, a known tooth initiation marker, as a direct target of Wnt/β-catenin signaling. These studies identify key mechanistic features responsible for supernumerary tooth formation.

Key words: Apc, Wnt, β-catenin, Fgf8, Msx1, Stem cells, Tooth regeneration

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