Analysis for a neural differentiation regulatory factor, Musashi1

2014 Fiscal Year Final Research Report

• Project/Area Number: 24500447
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurochemistry/Neuropharmacology
• Research Institution: Kyushu University (2013-2014); Keio University (2012)
• Principal Investigator: HORISAWA Kenichi 九州大学, 生体防御医学研究所, 助教 (70424207)
• Co-Investigator(Kenkyū-buntansha): 今井 貴雄 慶應義塾大学, 医学部生理学教室, 助教 (10383712) ; 芝田 晋介 慶應義塾大学, 医学部生理学教室, 講師 (70407089)
• Co-Investigator(Renkei-kenkyūsha): 岡野 栄之 慶應義塾大学, 医学部生理学教室, 教授 (60160694) ; 土居 信英 慶應義塾大学, 理工学部生命情報学科, 准教授 (50327673)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: Musashi1 / RNA結合タンパク質 / 神経発生 / 神経回路 / 未分化維持 / 翻訳制御 / 転写後制御 / 神経分化

Outline of Final Research Achievements

Musashi1 (Msi1) is a RNA-binding, which is highly expressed in neural stem/progenitor cells and is responsible for stem cell maintenance and differentiation. The main function of Msi1 is to regulate the expression of its target mRNAs through translational up/down-regulation.
In search for novel Msi1 targets, in vitro SELEX selection was performed from a mouse embryonic brain mRNA library, and a 3’ UTR fragment of dcc was obtained. Dcc is a transmembrane receptor expressed on the growth cones of neurons, and it guides axons and cells in response to Netrin1.
In this project, in vitro and in cultured cell experiments clearly identified that the dcc mRNA is a direct target of Msi1, and is suppressed their translation through a canonical molecular machinery. Now, we are analyzing the connection between the molecular mechanism and neural development by using Msi1-KO mice.

Free Research Field

分子生物学