中文摘要：

众所周知现代鸟类不长牙齿，而其侏罗纪和白垩纪的祖先则长有牙齿。然而，在发育中鸡胚口腔中却残留着牙齿发生的原基，在形态上与哺乳动物臼牙牙原基极为相似。现代鸟类的胚胎组织是否具有牙齿发育的潜能，目前已有不少研究者对这一问题进行了探讨。Kollar和Fisher 等人将鸡胚胎下颌靠近口腔面的上皮与小鼠的牙间充质进行组织重组实验，并植入小鼠眼球中作intraocular grafting培养。他们的实验结果表明重组后的组织块可以发育形成牙齿的结构，包括形成成釉细胞(ameloblast)，并能分泌釉质。Kollar等认为在进化过程中鸟类牙齿的消失并非由于口腔上皮中有关釉质合成的遗传信息的丢失，而是牙齿发育过程中的组织之间所必须的相互作用(次级诱导)受阻而造成的。Lemus和Fuenzalida等人的实验结果进一步证实了这一结论。他们用鹌鹑胚胎躯体的上皮组织与蜥蚁或兔子的牙间充质重组后，用鸡胚绒毛膜法进行培养，得到了发育很好的牙齿结构。发现鹌鹑的上皮细胞也可以分化形成釉质细胞，并分泌牙釉质。Cummings 将鹌鹑胚胎的牙上皮组织与小鼠胚胎的牙间充质组织重组后也得到类似的结果。根据小白鼠牙齿发育中已知的调控分子信号通路，我们曾对鸟类不长牙齿的分子机制进行了研究。我们的研究发现鸟类牙胚组织仍保留

英文摘要：

It is well known that modern Aves lack dentition, unlike their toothed ancestors of the Jurassic and cretaceous periods. However, in the chick oral cavity a rudiment forms that resembles the lamina stage of the mammalian molar tooth germ. We have previously 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. In this study, we further examined the molecular pathways involved in positioning the site of tooth rudiment. Similar to the mouse tooth germ, Pax9 serves as a marker for the presumptive dental mesenchyme in the chick prior to any morphological manifestation of odontogenesis. The restricted Pax9 expression in the chick mandibular mesenchyme is positioned by the two signals from overlying oral epithelium. FGF8 induces Pax9 expression while BMP4 prevents this induction. Thus it appears that, similar to that in mice, the position of tooth rudiment in chick embryo is determined by two different types of signaling molecules with antagonistic activity. These results further demonstrate that the early signaling pathways involved in odontogenesis remain inducible in Aves.