{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,4]],"date-time":"2026-06-04T23:10:15Z","timestamp":1780614615811,"version":"3.54.1"},"reference-count":49,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2010,2,1]],"date-time":"2010-02-01T00:00:00Z","timestamp":1264982400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2010,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Coordinated differentiation of the ameloblast cell layer is essential to enamel matrix protein deposition and subsequent mineralization. It has been hypothesized that this process is governed by Cx43\u2010based gap junctional intercellular communication as oculodentodigital dysplasia (ODDD) patients harboring autosomal\u2010dominant mutations in Cx43 exhibit enamel defects typically resulting in early adulthood tooth loss. To assess the role of Cx43 in tooth development we employ a mouse model of ODDD that harbors a G60S Cx43 mutant,<jats:italic>Gja1<\/jats:italic><jats:sup><jats:italic>Jrt<\/jats:italic><\/jats:sup><jats:italic>\/+<\/jats:italic>, and appears to exhibit tooth abnormalities that mimic the human disease. We found that total Cx43 plaques at all stages of ameloblast differentiation, as well as within the supporting cell layers, were greatly reduced in<jats:italic>Gja1<\/jats:italic><jats:sup><jats:italic>Jrt<\/jats:italic><\/jats:sup><jats:italic>\/+<\/jats:italic>incisors compared to wild\u2010type littermate controls. To characterize the<jats:italic>Gja1<\/jats:italic><jats:sup><jats:italic>Jrt<\/jats:italic><\/jats:sup><jats:italic>\/+<\/jats:italic>mouse tooth phenotype, mice were sacrificed prior to tooth eruption (postnatal day 7), weaning (postnatal day 21), and adulthood (2 months postnatal). A severely disorganized<jats:italic>Gja1<\/jats:italic><jats:sup><jats:italic>Jrt<\/jats:italic><\/jats:sup><jats:italic>\/+<\/jats:italic>mouse ameloblast layer and abnormal accumulation of amelogenin were observed at stages when the cells were active in secretion and mineralization. Differences in enamel thickness became more apparent after tooth eruption and incisor exposure to the oral cavity suggesting that enamel integrity is compromised, leading to rapid erosion. Additional analysis of incisors from mutant mice revealed that they were longer with a thicker dentin layer than their wild\u2010type littermates, which may reflect a mechanical stress response to the depleted enamel layer. Together, these data show that reduced levels of Cx43 gap junctions result in ameloblast dysregulation, enamel hypoplasia, and secondary tissue responses. J. Cell. Physiol. 223:601\u2013609, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jcp.22046","type":"journal-article","created":{"date-parts":[[2010,2,1]],"date-time":"2010-02-01T14:06:41Z","timestamp":1265033201000},"page":"601-609","source":"Crossref","is-referenced-by-count":37,"title":["Decreased levels of Cx43 gap junctions result in ameloblast dysregulation and enamel hypoplasia 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