Ikeda Keiko, Ookawara Shigeo, Sato Shigeru, Ando Zen-ichi, Kageyama Ryoichiro, Kawakami Kiyoshi
Division of Biology, Center for Molecular Medicine, Jichi Medical University, Shimotsuke, Tochigi 329-0498, Japan.
Dev Biol. 2007 Nov 1;311(1):53-68. doi: 10.1016/j.ydbio.2007.08.020. Epub 2007 Aug 16.
The olfactory epithelium (OE) is derived from the olfactory placode (OP) during mouse development. At embryonic day (E) 10.0-E10.5, "early neurogenesis" occurs in the OE, which includes production of pioneer neurons that emigrate out of the OE and other early-differentiated neurons. Around E12.5, the OE becomes organized into mature pseudostratified epithelium and shows "established neurogenesis," in which olfactory receptor neurons (ORNs) are differentiated from basal progenitors. Little is known about the molecular pathway of early neurogenesis. The homeodomain protein Six1 is expressed in all OP cells and neurogenic precursors in the OE. Here we show that early neurogenesis is severely disturbed despite the unaltered expression of Mash1 at E10.5 in the Six1-deficient mice (Six1-/-). Expression levels of neurogenin1 (Ngn1) and NeuroD are reduced and those of Hes1 and Hes5 are augmented in the OE of Six1-/- at E10.5. Pioneer neurons and cellular aggregates, which are derived from the OP/OE and situated in the mesenchyme between the OE and forebrain, are completely absent in Six1-/-. Moreover, ORN axons and the gonadotropin-releasing hormone-positive neurons fail to extend and migrate to the forebrain, respectively. Our study indicates that Six1 plays critical roles in early neurogenesis by regulating Ngn1, NeuroD, Hes1, and Hes5.
在小鼠发育过程中,嗅觉上皮(OE)源自嗅觉基板(OP)。在胚胎第10.0天至10.5天,OE中发生“早期神经发生”,其中包括产生从OE迁出的先驱神经元和其他早期分化的神经元。在大约胚胎第12.5天,OE组织成成熟的假复层上皮,并表现出“既定神经发生”,其中嗅觉受体神经元(ORN)从基底祖细胞分化而来。关于早期神经发生的分子途径知之甚少。同源结构域蛋白Six1在所有OP细胞和OE中的神经发生前体中表达。在此我们表明,尽管Six1基因缺陷小鼠(Six1-/-)在胚胎第10.5天Mash1的表达未改变,但早期神经发生仍受到严重干扰。在胚胎第10.5天Six1-/-的OE中,神经生成素1(Ngn1)和NeuroD的表达水平降低,而Hes1和Hes5的表达水平升高。源自OP/OE并位于OE和前脑之间间充质中的先驱神经元和细胞聚集体在Six1-/-中完全缺失。此外,ORN轴突和促性腺激素释放激素阳性神经元分别无法延伸和迁移至前脑。我们的研究表明,Six1通过调节Ngn1、NeuroD、Hes1和Hes5在早期神经发生中起关键作用。