| Project/Area Number |
17K15603
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General medical chemistry
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| Research Institution | Osaka City University |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 神経発生 / 微小管モータータンパク質 / 神経科学 / 細胞・組織 / 発生・分化 |
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| Outline of Final Research Achievements |
NudC was recently identified to regulate the distribution of motor protein on microtubules in neuron. This research was performed to clarify the function of NudC in developing central nervous system by using NudC conditional knockout (CKO) mice. We crossed NudC CKO mice with tau-cre transgenic mice to generate developing neuron-specific NudC deficient-mice (KO mice) and observed cerebral cortex morphology and layered structure of NudC KO embryos. We found that NudC-deficiency affected the distance of radial migration of neural progenitor cells but not proliferation and differentiation in embryonic cerebral cortex, which resulted in thinner cortical plate in NudC KO mice compared to wild type mice. Since cytoplasmic dynein, microtubule motor protein, is associated with neural progenitor migration in developing cortex, we suggest that NudC also controls the correct functions of motor protein in cortex development as well as axonal transport.
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| Academic Significance and Societal Importance of the Research Achievements |
NudCが属するNudファミリーでは、NudAが細胞質ダイニンに、NudFがLIS1に対応している。LIS1は細胞質ダイニンの制御因子であり、大脳皮質神経細胞の遊走障害によって起こる滑脳症の原因遺伝子でもある。これまでNudCの機能についてはあまり注目されてこなかったが、本研究によってNudCも大脳皮質の発生に重要な因子であることがはじめて明らかとなった。この成果が、滑脳症をはじめとする皮質層構造形成異常の機構解明の足がかりとなり、神経変性疾患のメカニズム解明に資する可能性が期待される。
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