On the difficulty of increasing dental complexity
On the difficulty of increasing dental complexity
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DOI：
10.1038/nature10876
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发表时间：
2012-03-15
期刊：
影响因子：
64.8
通讯作者：
Jernvall, Jukka
中科院分区：
文献类型：
--
作者：
Harjunmaa, Enni;Kallonen, Aki;Jernvall, Jukka
生命史的一个令人着迷的方面是形态复杂性随着时间的推移而明显增加(1)，一个众所周知的例子是哺乳动物颊齿的进化(2-4)。相比之下，发育的实验研究更容易显示复杂性的降低，哺乳动物牙齿也很好地证明了这一点，其中称为牙尖的牙冠特征在突变体和转基因小鼠中经常丢失(5-7)。在这里，我们报告说，通过同时调整多个信号通路可以大大增加小鼠牙齿的复杂性。我们在体外培养牙齿，并调整了外胚层增生素 (EDA)、激活素 A 和音刺猬 (SHH) 途径，所有这些途径都是正常牙齿发育所必需的。我们使用牙尖数量和表面复杂性的地形测量来量化牙齿的复杂性(8)。结果表明，虽然 EDA 和激活素 A 信号传导的激活以及 SHH 信号传导的抑制分别会导致复杂性的微妙至中度增加，但当所有三个途径同时调整时，尖点数量会增加一倍。此外，牙尖数量的增加并不是由于牙齿尺寸的增加，而是由于发育的初级图案阶段的改变。缺乏复杂突变体 (5-7)、缺乏具有复杂表型的自然变体 (9)，以及我们使用多种途径大大增加牙齿复杂性的结果，表明表型复杂性的增加可能本质上不同于表型复杂性的降低。
One of the fascinating aspects of the history of life is the apparent increase in morphological complexity through time(1), a well known example being mammalian cheek tooth evolution(2-4). In contrast, experimental studies of development more readily show a decrease in complexity, again well exemplified by mammalian teeth, in which tooth crown features called cusps are frequently lost in mutant and transgenic mice(5-7). Here we report that mouse tooth complexity can be increased substantially by adjusting multiple signalling pathways simultaneously. We cultured teeth in vitro and adjusted ectodysplasin (EDA), activin A and sonic hedgehog (SHH) pathways, all of which are individually required for normal tooth development. We quantified tooth complexity using the number of cusps and a topographic measure of surface complexity(8). The results show that whereas activation of EDA and activin A signalling, and inhibition of SHH signalling, individually cause subtle to moderate increases in complexity, cusp number is doubled when all three pathways are adjusted in unison. Furthermore, the increase in cusp number does not result from an increase in tooth size, but from an altered primary patterning phase of development. The combination of a lack of complex mutants(5-7), the paucity of natural variants with complex phenotypes(9), and our results of greatly increased dental complexity using multiple pathways, suggests that an increase may be inherently different from a decrease in phenotypic complexity.