Zhulyn Olena, Hui Chi-Chung
Program in Developmental and Stem Cell Biology, The Hospital for Sick Children, Toronto, Ontario, Canada; Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada.
Dev Dyn. 2015 Mar;244(3):468-78. doi: 10.1002/dvdy.24249. Epub 2015 Jan 24.
The vertebrate digit pattern is defined by the morphogen Sonic hedgehog (Shh), which controls the activity of Gli transcription factors. Gli1, 2 and 3 are dynamically expressed during patterning. Downstream of Shh, their activity is regulated by Sufu and Kif7, core components of the Shh signaling cascade. The precise roles of these regulators during limb development have not been fully described. We analyze the role of Sufu and Kif7 in the limb and demonstrate that their loss has distinct and synergistic effects on Gli activity and digit pattern.
Using a series of mouse mutants, we show that Sufu and Kif7 are expressed throughout limb development and their deletion has distinct effects on Gli levels and limb formation. Concomitant deletion of Sufu and Kif7 results in constitutive pathway activity and severe limb truncation. This is consistent with the recently published two-population model, which suggests that precocious activation of Shh signaling inhibits organizing center formation and limb outgrowth.
Together, our findings demonstrate that perturbations of Sufu and Kif7 affect Gli activity and recapitulate the full spectrum of vertebrate limb defects, ranging from severe truncation to polydactyly.
脊椎动物的指(趾)模式由形态发生素音猬因子(Shh)定义,Shh控制Gli转录因子的活性。Gli1、2和3在模式形成过程中动态表达。在Shh的下游,它们的活性受抑制因子(Sufu)和驱动蛋白7(Kif7)调节,这两者是Shh信号级联反应的核心成分。这些调节因子在肢体发育过程中的精确作用尚未得到充分描述。我们分析了Sufu和Kif7在肢体中的作用,并证明它们的缺失对Gli活性和指(趾)模式有不同的协同效应。
使用一系列小鼠突变体,我们发现Sufu和Kif7在整个肢体发育过程中均有表达,它们的缺失对Gli水平和肢体形成有不同影响。Sufu和Kif7的同时缺失导致组成型信号通路激活和严重的肢体截断。这与最近发表的双群体模型一致,该模型表明Shh信号的过早激活会抑制组织中心的形成和肢体生长。
总之,我们的研究结果表明,Sufu和Kif7的扰动会影响Gli活性,并概括了脊椎动物肢体缺陷的全谱,从严重截断到多指(趾)畸形。