| Project/Area Number |
15K08148
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
General anatomy (including histology/embryology)
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Research Collaborator |
OOTA motonori 名古屋大学, 情報学研究科, 教授 (40290895)
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| Project Period (FY) |
2015-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 細胞・組織 / 軸索ガイダンス / バイオインフォマティクス / 末梢神経 / 神経変性疾患 / 細胞分化・組織形成 |
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| Outline of Final Research Achievements |
Axons in higher vertebrates can reach the appropriate targets by attractive and repulsive axonal guidance cues in vivo. We found that two novel secretory molecules (mF1 and mF2) play an important role in axonal guidance. In this study, we determined the domain structures of each molecule by bioinformatics, and then selected candidate receptor molecules using our prediction methods of gene function. In addition, we identified the expression regions of mF1 and mF2 mRNA in mouse embryos by in situ hybridization, and determined the functional domains in axonal guidance using site-directed mutagenesis methods.
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| Academic Significance and Societal Importance of the Research Achievements |
神経の軸索を反発する分子についてはこれまでに多くの報告がある．しかしながら，軸索反発因子と比較して，軸索誘引因子に関する報告は極めて少ない．DRGの神経軸索を誘引する分子メカニズムを解明できれば，世界に先駆けた発見となり，神経科学における意義は大きい．また，DRG軸索は神経損傷の好発部位である末梢神経の感覚線維を構成している．DRG軸索を誘引・反発する因子は，神経損傷および神経変性疾患に対する治療剤としての適応が可能であり，臨床研究および神経再生治療にも大きな影響を及ぼしうる．
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