An analysis of mechanism of neural tube closure using the SIP1 knock-out mice as a spina bifida model

本研究旨在阐明神经管闭合缺陷的发生机制。为此，我们将SIP1基因敲除的小鼠作为脊柱裂的模型进行分析。几个参与神经管收缩的分子的顶端定位不足。未观察到SIP1基因敲除胚胎神经管背侧Smad5的磷酸化。SIP1基因敲除胚胎的部分神经外胚层细胞异常分化，转化为具有泡状形态的上皮样细胞。这些结果为SIP1在神经管闭合中的未知功能提供了一些见解，神经管闭合是脊柱裂的一个基本生物学过程。

The aim of this study is to elucidate the mechanism of neural tube closure defects. For this purpose, we analyze the SIP1 knock-out mice as a spina bifida model. The apical localization of several molecules participating neural tube contraction were found to be insufficient. The phosphorylation of Smad5 on the dorsal side of the neural tube of the SIP1 knock-out embryo was not observed. A part of the neural ectoderm cells of the SIP1 knock-out embryo abnormally differentiated and transformed into the epithelial-like cells with a bleb morphology. These results give some insights into the unknown function of SIP1 in neural tube closure, a fundamental biological process harboring etiologies of spina bifida.