Conservation of early odontogenic signaling pathways in Aves
Conservation of early odontogenic signaling pathways in Aves
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DOI：
10.1073/pnas.160245097
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发表时间：
2000-08-29
影响因子：
11.1
通讯作者：
Maas, R
中科院分区：
文献类型：
--
作者：
Chen, YP;Zhang, YD;Maas, R
鸟类的牙齿已经消失了至少6000万年。然而，在鸡口腔中形成的雏形类似于哺乳动物臼齿牙胚的薄层阶段。我们通过分析鸡胚中已知调节小鼠牙齿发育的分子途径的状态，解决了鸟类牙齿形成继发性丧失的分子基础。与小鼠牙板相似，Fgf8、Pitx 2、Barx 1和Pax 9的表达定义了一个潜在的鸡牙源性区域。然而，参与牙齿起始的三种分子Bmp4、Msx1和Msx2的表达在假定的鸡牙板中不存在。在鸡下颌骨中，外源性骨形态发生蛋白（BMP）诱导Msx表达，并与成纤维细胞生长因子一起促进表达Sonic hedgehog的上皮结构的发育。当鸡下颌上皮与骨形态发生蛋白和成纤维细胞生长因子的组织来源鸡皮肤间充质重组时，也诱导了明显的上皮附属物。这些结果表明，虽然潜伏的，早期信号通路参与牙发育仍然是诱导的鸟类，并建议牙源性Bmp4表达的损失可能是负责在活禽牙齿发育的早期逮捕。
Teeth have been missing from birds (Aves) for at least 60 million years. However, in the chick oral cavity a rudiment forms that resembles the lamina stage of the mammalian molar tooth germ. We have addressed the molecular basis for this secondary loss of tooth formation in Aves by analyzing in chick embryos the status of molecular pathways known to regulate mouse tooth development. Similar to the mouse dental lamina, expression of Fgf8, Pitx2, Barx1, and Pax9 defines a potential chick odontogenic region. However, the expression of three molecules involved in tooth initiation, Bmp4, Msx1, and Msx2, are absent from the presumptive chick dental lamina. In chick mandibles, exogenous bone morphogenetic protein (BMP) induces Msx expression and together with fibroblast growth factor promotes the development of Sonic hedgehog expressing epithelial structures. Distinct epithelial appendages also were induced when chick mandibular epithelium was recombined with a tissue source of BMPs and fibroblast growth factors, chick skin mesenchyme. These results show that, although latent, the early signaling pathways involved in odontogenesis remain inducible in Aves and suggest that loss of odontogenic Bmp4 expression may be responsible for the early arrest of tooth development in living birds.