2013 Fiscal Year Final Research Report

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

Research Project

Project/Area Number	23791215
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Pediatrics
Research Institution	Institute for Developmental Research, Aichi Human Service Center
Principal Investigator	NISHIZAKI Yuriko 愛知県心身障害者コロニー発達障害研究所, 周生期学部, リサーチレジデント (90378901)
Project Period (FY)	2011 – 2012
Keywords	SIP1 / 神経管閉鎖 / 二分脊椎症
Research Abstract	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.