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J. Biol. Chem., Vol. 283, Issue 22, 15056-15062, May 30, 2008

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Partial Rescue of the Amelogenin Null Dental Enamel Phenotype^*

Yong Li, Cynthia Suggs, J. Timothy Wright, Zhi-an Yuan, Melissa Aragon, Hanson Fong^¶, Darrin Simmons, Bill Daly, Ellis E. Golub^||, Gerald Harrison^||, Ashok B. Kulkarni^**, and Carolyn W. Gibson¹

From the Departments of Anatomy and Cell Biology and ^||Biochemistry, University of Pennsylvania School of Dental Medicine, Philadelphia, Pennsylvania 19104-6030, the Department of Pediatric Dentistry, University of North Carolina, School of Dentistry, Chapel Hill, North Carolina 27599, the ^¶Department of Materials Science and Engineering, University of Washington, Seattle, Washington 98195, and the ^**Functional Genomics Section, Laboratory of Cell and Developmental Biology, NIDCR, National Institutes of Health, Bethesda, Maryland 20892

The amelogenins are the most abundant secreted proteins in developing dental enamel. Enamel from amelogenin (Amelx) null mice is hypoplastic and disorganized, similar to that observed in X-linked forms of the human enamel defect amelogenesis imperfecta resulting from amelogenin gene mutations. Both transgenic strains that express the most abundant amelogenin (TgM180) have relatively normal enamel, but strains of mice that express a mutated amelogenin (TgP70T), which leads to amelogenesis imperfecta in humans, have heterogeneous enamel structures. When Amelx null (KO) mice were mated with transgenic mice that produce M180 (TgM180), the resultant TgM180KO offspring showed evidence of rescue in enamel thickness, mineral density, and volume in molar teeth. Rescue was not observed in the molars from the TgP70TKO mice. It was concluded that a single amelogenin protein was able to significantly rescue the KO phenotype and that one amino acid change abrogated this function during development.

Received for publication, September 25, 2007 , and in revised form, March 7, 2008.

^* This work was authored, in whole or in part, by National Institutes of Health staff. This work was supported by NIDCR National Institutes of Health Grant DE011089 (to C. W. G.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The Amelx null strain was deposited with the Jackson Laboratory (Bar Harbor, ME), and transgenic strains generated at the University of Pennsylvania Transgenic Core Facility were deposited with the MMRRC (Mutant Mouse Region Resource Center).

¹ To whom correspondence should be addressed: Dept. of Anatomy and Cell Biology, University of Pennsylvania School of Dental Medicine, 240 S. 40th St., Philadelphia, PA 19104-6030. Tel.: 215-898-6660; Fax: 215-573-2324; E-mail: gibson{at}biochem.dental.upenn.edu.

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				J. Hatakeyama, S. Fukumoto, T. Nakamura, N. Haruyama, S. Suzuki, Y. Hatakeyama, L. Shum, C. W. Gibson, Y. Yamada, and A. B. Kulkarni Synergistic Roles of Amelogenin and Ameloblastin Journal of Dental Research, April 1, 2009; 88(4): 318 - 322. [Abstract] [Full Text] [PDF]