Human Molecular Genetics Advance Access originally published online on August 14, 2008
Human Molecular Genetics 2008 17(22):3509-3520; doi:10.1093/hmg/ddn243
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
The cell adhesion molecule nectin-1 is critical for normal enamel formation in mice
1 Faculty of Life Sciences 2 Dental School, University of Manchester, Michael Smith Building, Oxford Road, Manchester M13 9PT, UK 3 Department of Oral Biology, Leeds Dental Institute, University of Leeds, Clarendon Way, Leeds LS2 9LU, UK
* To whom correspondence should be addressed. +44 161 275 5620; Fax: +44 161 275 5082; Email: mike.dixon{at}manchester.ac.uk
Received July 6, 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 mice lacking nectin-1 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 maturation-stage ameloblasts and the underlying cells of the stratum intermedium (SI), 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 SI–ameloblast interface is essential for normal enamel mineralization.