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首页> 外文期刊>Development >Regulation of tooth number by fine-tuning levels of receptor-tyrosine kinase signaling.
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Regulation of tooth number by fine-tuning levels of receptor-tyrosine kinase signaling.

机译：通过微调受体酪氨酸激酶信号传导水平来调节牙齿数量。

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Much of our knowledge about mammalian evolution comes from examination of dental fossils, because the highly calcified enamel that covers teeth causes them to be among the best-preserved organs. As mammals entered new ecological niches, many changes in tooth number occurred, presumably as adaptations to new diets. For example, in contrast to humans, who have two incisors in each dental quadrant, rodents only have one incisor per quadrant. The rodent incisor, because of its unusual morphogenesis and remarkable stem cell-based continuous growth, presents a quandary for evolutionary biologists, as its origin in the fossil record is difficult to trace, and the genetic regulation of incisor number remains a largely open question. Here, we studied a series of mice carrying mutations in sprouty genes, the protein products of which are antagonists of receptor-tyrosine kinase signaling. In sprouty loss-of-function mutants, splitting of gene expression domains and reduced apoptosis was associated with subdivision of the incisor primordium and a multiplication of its stem cell-containing regions. Interestingly, changes in sprouty gene dosage led to a graded change in incisor number, with progressive decreases in sprouty dosage leading to increasing numbers of teeth. Moreover, the independent development of two incisors in mutants with large decreases in sprouty dosage mimicked the likely condition of rodent ancestors. Together, our findings indicate that altering genetic dosage of an antagonist can recapitulate ancestral dental characters, and that tooth number can be progressively regulated by changing levels of activity of a single signal transduction pathway.
机译：我们对哺乳动物进化的许多知识都来自对牙齿化石的检查，因为覆盖牙齿的高度钙化的珐琅质使其成为保存最完好的器官之一。当哺乳动物进入新的生态位时，牙齿数量发生了许多变化，大概是因为它们适应了新的饮食。例如，与在每个象限中都有两个门牙的人类相反，啮齿动物在每个象限中只有一个门牙。啮齿动物的切牙由于其异常的形态发生和显着的基于干细胞的连续生长，对进化生物学家提出了难题，因为其在化石记录中的起源很难追踪，并且切牙数目的遗传调控仍然是一个很大的问题。在这里，我们研究了一系列在发芽基因中携带突变的小鼠，其蛋白质产物是受体酪氨酸激酶信号转导的拮抗剂。在发芽的功能丧失型突变体中，基因表达域的分裂和细胞凋亡的减少与切牙原基的细分及其含干细胞区域的繁殖有关。有趣的是，发芽基因剂量的变化导致门牙数目的分级变化，发芽剂量的逐渐减少导致牙齿数目的增加。此外，发芽剂量大幅度降低的突变体中两个切齿的独立发育模仿了啮齿动物祖先的可能状况。总之，我们的发现表明，改变拮抗剂的遗传剂量可以概括祖先的牙齿特征，并且可以通过改变单个信号转导途径的活性水平来逐步调节牙齿的数量。

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