Laminin gamma2 expression is developmentally regulated during murine tooth morphogenesis and is intense in ameloblasts.

Mutations in the laminin gamma2 gene cause junctional epidermolysis bullosa, and enamel hypoplasias are frequently seen in these patients. Laminin gamma2 is one of the three polypeptide chains forming the basement membrane glycoprotein laminin-5. We have localized the expression of the laminin gamma2 gene by in situ hybridization during mouse tooth development from early morphogenesis to completion of crown development. The expression was restricted to epithelial cells. During the early morphogenesis of the tooth germ, laminin gamma2 was expressed by the outer dental epithelium and by the stellate reticulum cells. No expression was detected in the cells of the inner dental epithelium giving rise to ameloblasts. The pre-ameloblasts remained negative during the early bell stage, but, interestingly, expression was very prominently upregulated as the cells differentiated into ameloblasts. This upregulation appeared to coincide with the start of enamel matrix secretion. The ameloblasts expressed laminin gamma2 intensely throughout the period of active enamel deposition. The expression continued at a lower level in the maturation-stage ameloblasts covering the enamel surface. Immunolocalization of laminin-5 with polyclonal antibodies indicated that the protein formed a continuous lining at the basal surfaces of the cells expressing the laminin gamma2 transcripts. We suggest that the role of laminin-5 during enamel formation may be to strengthen the anchorage of the ameloblasts to the enamel matrix, and that the pathogenesis of enamel hypoplasias in cases of laminin-5 mutations could be associated with detachment of the ameloblast cell layer from the enamel surface.