2012 Fiscal Year Final Research Report
Analyses on the pathogenesis of L1-associated hydrocephalus by knocking down L1 and TAG-1
Project/Area Number |
22390214
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Research Category |
Grant-in-Aid for Scientific Research (B)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Embryonic/Neonatal medicine
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Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
ITOH Kyoko 京都府立医科大学, 医学研究科, 准教授 (80243301)
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Co-Investigator(Kenkyū-buntansha) |
FUSHIKI Shinji 京都府立医科大学, 医学研究科, 教授 (80150572)
YAOI Takeshi 京都府立医科大学, 医学研究科, 助教 (40311914)
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Project Period (FY) |
2010 – 2012
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Keywords | 先天異常学 / 胎児性水頭症 / L1CAM |
Research Abstract |
L1 is a cell adhesion molecule associated with a spectrum of human neurological diseases, however; the function of L1 in neuronal migration during cortical histogenesis remains to be clarified. We therefore investigated the corticogenesis of mice embryos where L1 molecules were knocked down (L1-KD) in selected neurons, employing in utero electroporation with shRNAs targeting L1 (L1-shRNA). The radial migration of L1-KD neurons was significantly delayed and the directions of the leading process of L1-KD neurons became more dispersed, compared with the control neurons. In addition, two transcription factors expressed in the neurons, Satb2 and Tbr1, were shown to be reduced or aberrantly expressed in L1-KD neurons. These observations suggest that L1 plays an important role in regulating the locomotion and orientation of migrating neurons and the expression of transcription factors during neocortical development.
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Research Products
(4 results)