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Human Molecular Genetics Advance Access published online on August 14, 2008

Human Molecular Genetics, doi:10.1093/hmg/ddn243
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© 2008 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

The cell adhesion molecule nectin-1 is critical for normal enamel formation in mice

Martin J. Barron1,2, Steven J. Brookes3, Clare E. Draper1, David Garrod1, Jennifer Kirkham3, Roger C. Shore3 and Michael J. Dixon1,2,*

1 Faculty of Life Sciences, Michael Smith Building, University of Manchester, Oxford Road, Manchester M13 9PT, UK 2 Dental School, Michael Smith Building, University of Manchester, Oxford Road, Manchester, M13 9PT, UK 3 Department of Oral Biology, Leeds Dental Institute, University of Leeds, Clarendon Way, Leeds LS2 9LU, UK

* Corresponding author: E-mail: mike.dixon{at}manchester.ac.uk; Telephone number: +44-161 275 5620; Fax: +44-161 275 5082

Received July 6, 2008; Revised August 12, 2008; Accepted August 12, 2008

Nectin-1 is a member of a sub-family of immunoglobulin-like adhesion molecules and a component of adherens junctions. In the current study, we have shown that lacking nectin-1 mice exhibit defective enamel formation in their incisor teeth. Although the incisors of nectin-1-null mice were hypomineralized, the protein composition of the enamel matrix was unaltered. While strong immunostaining for nectin-1 was observed at the interface between the mature ameloblasts and the underlying cells of the stratum intermedium, its absence in nectin-1-null mice correlated with separation of the cell layers at this interface. Numerous, large desmosomes were present at this interface in wild-type mice; however, where adhesion persisted in the mutant mice, the desmosomes were smaller and less numerous. Nectins have been shown to regulate tight junction formation; however, this is the first report showing that they may also participate in the regulation of desmosome assembly. Importantly, our results show that integrity of the stratum intermedium-ameloblast interface is essential for normal enamel mineralization.


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