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Published online on November 22, 2006, 10.1073/pnas.0607289103
PNAS | December 5, 2006 | vol. 103 | no. 49 | 18627-18632


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BIOLOGICAL SCIENCE / DEVELOPMENTAL BIOLOGY
Continuous tooth generation in mouse is induced by activated epithelial Wnt/beta-catenin signaling

Elina Järvinen*, Isaac Salazar-Ciudad*, Walter Birchmeier{dagger}, Makoto M. Taketo{ddagger}, Jukka Jernvall*, and Irma Thesleff*,§

*Developmental Biology Program, Institute of Biotechnology, Viikki Biocenter, P.O. Box 56, University of Helsinki, FIN-00014, Helsinki, Finland; {dagger}Max-Delbrueck-Center for Molecular Medicine, Robert-Roessle-Strasse 10, 13092 Berlin, Germany; and {ddagger}Department of Pharmacology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, Kyoto 606-8501, Japan

Edited by Eric N. Olson, University of Texas Southwestern Medical Center, Dallas, TX, and approved October 3, 2006 (received for review August 22, 2006)

The single replacement from milk teeth to permanent teeth makes mammalian teeth different from teeth of most nonmammalian vertebrates and other epithelial organs such as hair and feathers, whose continuous replacement has been linked to Wnt signaling. Here we show that mouse tooth buds expressing stabilized beta-catenin in epithelium give rise to dozens of teeth. The molar crowns, however, are typically simplified unicusped cones. We demonstrate that the supernumerary teeth develop by a renewal process where new signaling centers, the enamel knots, bud off from the existing dental epithelium. The basic aspects of the unlocked tooth renewal can be reproduced with a computer model on tooth development by increasing the intrinsic level of activator production, supporting the role of beta-catenin pathway as an upstream activator of enamel knot formation. These results may implicate Wnt signaling in tooth renewal, a capacity that was all but lost when mammals evolved progressively more complicated tooth shapes.

organ renewal | regeneration | tooth development | activator-inhibitor model

Author contributions: E.J., J.J., and I.T. designed research; E.J. and I.S.-C. performed research; W.B. and M.M.T. contributed new reagents/analytic tools; E.J., J.J., and I.T. analyzed data; and E.J., J.J., and I.T. wrote the paper.

The authors declare no conflict of interest.

This article is a PNAS direct submission.

This article contains supporting information online at www.pnas.org/cgi/content/full/0607289103/DC1.

§To whom correspondence should be addressed. E-mail: irma.thesleff{at}helsinki.fi

© 2006 by The National Academy of Sciences of the USA


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