Litingtung Ying, Dahn Randall D, Li Yina, Fallon John F, Chiang Chin
Vanderbilt University Medical Center, Department of Cell and Developmental Biology, Nashville, Tennessee 37232, USA.
Nature. 2002 Aug 29;418(6901):979-83. doi: 10.1038/nature01033. Epub 2002 Aug 18.
Most current models propose Sonic hedgehog (Shh) as the primary determinant of anteroposterior development of amniote limbs. Shh protein is said to be required to direct the formation of skeletal elements and to specify digit identity through dose-dependent activation of target gene expression. However, the identity of genes targeted by Shh, and the regulatory mechanisms controlling their expression, remain poorly understood. Gli3 (the gene implicated in human Greig cephalopolysyndactyly syndrome) is proposed to negatively regulate Shh by restricting its expression and influence to the posterior mesoderm. Here we report genetic analyses in mice showing that Shh and Gli3 are dispensable for formation of limb skeletal elements: Shh(-/-) Gli3(-/-) limbs are distally complete and polydactylous, but completely lack wild-type digit identities. We show that the effects of Shh signalling on skeletal patterning and ridge maintenance are necessarily mediated through Gli3. We propose that the function of Shh and Gli3 in limb skeletal patterning is limited to refining autopodial morphology, imposing pentadactyl constraint on the limb's polydactyl potential, and organizing digit identity specification, by regulating the relative balance of Gli3 transcriptional activator and repressor activities.
目前大多数模型认为,音猬因子(Shh)是羊膜动物肢体前后轴发育的主要决定因素。据说Shh蛋白对于指导骨骼元件的形成以及通过剂量依赖性激活靶基因表达来确定指(趾)身份是必需的。然而,Shh靶向的基因的身份以及控制其表达的调控机制仍知之甚少。Gli3(与人类Greig头多指综合征相关的基因)被认为通过限制Shh的表达及其对后中胚层的影响来负向调节Shh。在此,我们报告了在小鼠中的遗传分析,结果表明Shh和Gli3对于肢体骨骼元件的形成并非必需:Shh(-/-) Gli3(-/-) 肢体在远端是完整的且多指,但完全缺乏野生型指(趾)身份。我们表明,Shh信号对骨骼模式形成和嵴维持的影响必然是通过Gli3介导的。我们提出,Shh和Gli3在肢体骨骼模式形成中的功能仅限于通过调节Gli3转录激活剂和抑制剂活性的相对平衡来细化远节肢体形态、对肢体的多指潜能施加五指约束以及组织指(趾)身份的确定。