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

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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.