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

• Published in: Human molecular genetics 2008-11, Vol.17 (22), p.3509-3520
• Main Authors: Barron, Martin J., Brookes, Steven J., Draper, Clare E., Garrod, David, Kirkham, Jennifer, Shore, Roger C., Dixon, Michael J.
• Format: Article
• Language: English
• Subjects: Adherens junctions; Adherens Junctions - metabolism; Ameloblasts; Ameloblasts - cytology; Ameloblasts - physiology; Amelogenesis; Animals; Apoptosis; Biological and medical sciences; Cell Adhesion; Cell adhesion & migration; Cell adhesion molecules; Cell Adhesion Molecules - genetics; Cell Adhesion Molecules - metabolism; Cell Proliferation; Dental enamel; Dental Enamel - chemistry; Dental Enamel - metabolism; Dental Enamel Proteins - analysis; Desmoplakins - analysis; Desmosomes; Desmosomes - metabolism; Desmosomes - ultrastructure; Enamel; Enamel Organ - chemistry; Enamel Organ - cytology; Enamel Organ - metabolism; Extracellular matrix; Ferric Compounds - metabolism; Fundamental and applied biological sciences. Psychology; Genetics of eukaryotes. Biological and molecular evolution; Immunoglobulins; Immunohistochemistry; Incisor - abnormalities; Incisor - diagnostic imaging; Incisors; Mice; Mice, Transgenic; Microphthalmos; Microscopy, Electron, Transmission; Mineralization; Molecular and cellular biology; Mutation; Nectin; Nectins; Protein composition; Proteins; Radiography; Rodents; Stem cells; Teeth; Tight Junctions - metabolism; Tight Junctions - ultrastructure
• ISSN: 0964-6906; 1460-2083
• DOI: 10.1093/hmg/ddn243

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.