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J. Biol. Chem., Vol. 277, Issue 51, 49598-49604, December 20, 2002
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From the Enamelysin is a tooth-specific matrix
metalloproteinase that is expressed during the early through middle
stages of enamel development. The enamel matrix proteins amelogenin,
ameloblastin, and enamelin are also expressed during this same
approximate developmental time period, suggesting that enamelysin may
play a role in their hydrolysis. In support of this interpretation,
recombinant enamelysin was previously demonstrated to cleave
recombinant amelogenin at virtually all of the precise sites known to
occur in vivo. Thus, enamelysin is likely an important
amelogenin-processing enzyme. To characterize the in vivo
biological role of enamelysin during tooth development, we generated an
enamelysin-deficient mouse by gene targeting. Although mice
heterozygous for the mutation have no apparent phenotype, the
enamelysin null mouse has a severe and profound tooth phenotype.
Specifically, the null mouse does not process amelogenin properly,
possesses an altered enamel matrix and rod pattern, has hypoplastic
enamel that delaminates from the dentin, and has a deteriorating enamel
organ morphology as development progresses. Our findings demonstrate
that enamelysin activity is essential for proper enamel development.
Enamelysin (Matrix Metalloproteinase 20)-deficient Mice
Display an Amelogenesis Imperfecta Phenotype*
,,
,, and
Matrix Metalloproteinase Unit, NIDCR,
National Institutes of Health, Bethesda, Maryland 20892, the
§ Biostructure Core Facility and the ¶ Department of
Cytokine Biology, Forsyth Institute, Boston, Massachusetts 02115, Department of Biologic and Material Sciences, University of
Michigan School of Dentistry, Ann Arbor Michigan 48108, and the
** Department of Oral and Developmental Biology, Harvard
Medical School, Boston, Massachusetts 02115
*
This work was supported in part by NIDCR, National
Institutes of Health Grant DE14084 (to J. D. B.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Cytokine
Biology, Forsyth Institute, Boston MA 02115. Tel.: 617-262-5200 (ext.
388); Fax: 617-456-7732; E-mail: jbartlett@forsyth.org.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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