Department of Anatomy, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Dev Dyn. 2012 Aug;241(8):1289-300. doi: 10.1002/dvdy.23819. Epub 2012 Jun 22.
Hes1 gene represses the expression of proneural basic helix-loop-helix (bHLH) factor Mash1, which is essential for the differentiation of the sympathetic ganglia and carotid body glomus cells. The sympathetic ganglia, carotid body, and common carotid artery in Wnt1-Cre/R26R double transgenic mice were intensely labeled by X-gal staining, i.e., the neural crest origin. The deficiency of Hes1 caused severe hypoplasia of the superior cervical ganglion (SCG). At embryonic day (E) 17.5-E18.5, the volume of the SCG in Hes1 null mutants was reduced to 26.4% of the value in wild-type mice. In 4 of 30 cases (13.3%), the common carotid artery derived from the third arch artery was absent in the null mutants, and the carotid body was not formed. When the common carotid artery was retained, the organ grew in the wall of the third arch artery and glomus cell precursors were provided from the SCG in the null mutants as well as in wild-types. However, the volume of carotid body in the null mutants was only 52.5% of the value in wild-types at E17.5-E18.5. These results suggest that Hes1 plays a critical role in regulating the development of neural crest derivatives in the mouse cervical region.
Hes1 基因抑制了 proneural basic helix-loop-helix(bHLH) 因子 Mash1 的表达，后者对于交感神经节和颈动脉体球细胞的分化是必需的。在 Wnt1-Cre/R26R 双转基因小鼠中，交感神经节、颈动脉体和颈总动脉通过 X-gal 染色强烈标记，即神经嵴起源。Hes1 的缺失导致了上颈神经节（SCG）的严重发育不良。在胚胎期 17.5-18.5 天，Hes1 缺失突变体的 SCG 体积减少到野生型小鼠的 26.4%。在 30 例中的 4 例（13.3%）中，缺失突变体中第三弓动脉起源的颈总动脉缺失，颈动脉体未形成。当保留颈总动脉时，该器官在第三弓动脉的壁中生长，并且在缺失突变体和野生型中，球细胞前体均来自 SCG。然而，在 E17.5-E18.5 时，缺失突变体中颈动脉体的体积仅为野生型的 52.5%。这些结果表明 Hes1 在调节小鼠颈部神经嵴衍生物的发育中发挥着关键作用。
