Transgenic Rescue of Enamel Phenotype in Ambn Null Mice
Transgenic Rescue of Enamel Phenotype in Ambn Null Mice
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DOI：
10.1177/0022034510379223
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发表时间：
2010-12-01
影响因子：
7.6
通讯作者：
Simmer, J. P.
中科院分区：
文献类型：
--
作者：
Chun, Y. -H. P.;Lu, Y.;Simmer, J. P.
成釉蛋白基因敲除小鼠不能形成釉质层，但这种缺陷可能是由于功能性成釉蛋白的缺乏或潜在毒性突变成釉蛋白的分泌。我们假设，釉质表型可以拯救正常成釉蛋白的转基因表达在Ambn突变小鼠。我们建立并分析了5个转基因株系，这些转基因株系从釉原蛋白（AmelX）启动子表达成釉蛋白，并鉴定了几乎不表达转基因、略低于正常（Tg+）、略高于正常（Tg++）和远高于正常（Tg+）成釉蛋白水平的转基因株系。所有表达可检测水平的成釉蛋白的细胞系至少部分恢复了釉质表型。当成釉蛋白表达仅略高于正常时，覆盖磨牙和切牙的釉质具有正常厚度，具有明确的杆和杆间釉质，并且保持良好的功能。我们的结论是，成釉蛋白是必不可少的牙釉质形成。
Ameloblastin null mice fail to make an enamel layer, but the defects could be due to an absence of functional ameloblastin or to the secretion of a potentially toxic mutant ameloblastin. We hypothesized that the enamel phenotype could be rescued by the transgenic expression of normal ameloblastin in Ambn mutant mice. We established and analyzed 5 transgenic lines that expressed ameloblastin from the amelogenin (AmelX) promoter and identified transgenic lines that express virtually no transgene, slightly less than normal (Tg+), somewhat higher than normal (Tg++), and much higher than normal (Tg+++) levels of ameloblastin. All lines expressing detectable levels of ameloblastin at least partially recovered the enamel phenotype. When ameloblastin expression was only somewhat higher than normal, the enamel covering the molars and incisors was of normal thickness, had clearly defined rod and interrod enamel, and held up well in function. We conclude that ameloblastin is essential for dental enamel formation.