Barron Martin J, Brookes Steven J, Draper Clare E, Garrod David, Kirkham Jennifer, Shore Roger C, Dixon Michael J
Faculty of Life Sciences, University of Manchester, Manchester, UK.
Hum Mol Genet. 2008 Nov 15;17(22):3509-20. doi: 10.1093/hmg/ddn243. Epub 2008 Aug 14.
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.
Nectin-1是免疫球蛋白样粘附分子亚家族的成员，也是黏着连接的一个组成部分。在本研究中，我们发现缺乏Nectin-1的小鼠其门齿的釉质形成存在缺陷。尽管Nectin-1基因敲除小鼠的门齿矿化不足，但其釉质基质的蛋白质组成未发生改变。虽然在成熟阶段的成釉细胞与中间层（SI）下层细胞之间的界面处观察到Nectin-1有强烈的免疫染色，但在Nectin-1基因敲除小鼠中该界面处细胞层的分离与Nectin-1的缺失相关。在野生型小鼠的该界面处存在大量大的桥粒；然而，在突变小鼠中，尽管存在黏附，但桥粒更小且数量更少。已证明Nectins可调节紧密连接的形成；然而，这是首次报道表明它们可能也参与桥粒组装的调节。重要的是，我们的结果表明SI-成釉细胞界面的完整性对于正常的釉质矿化至关重要。
