| Project/Area Number |
07671540
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | JUNTENDO UNIVERSITY |
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Principal Investigator |
ARAI Hajime (1996-1997) Juntendo University School of Medicine Department of Neurosurgery Associatet Professor, 医学部, 助教授 (70167229)
須田 喜久夫 (1995) 順天堂大学, 医学部, 助手 (00206559)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAJIMA Masakazu Juntendo University School of Medicine Department of Neurosurgry Assistant Profe, 医学部, 講師 (60200177)
新井 一 順天堂大学, 医学部, 助教授 (70167229)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1997: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
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| Keywords | Helix-loop-helix transcription factor / chick embryo / neural tube / neurogenesis / molecular biology / Helix-loop-helix (HLH) transcription factor: / Helix-loop-helix transcription factors |
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| Research Abstract |
3Helix-loop-helix (HLH) transcription factors play a critical role in neural tube development. Three class A basic HLH transcription factors are present in the developing chick neural tube whereas GE1, GE12 is expressed in interneurons and not in motoneurons. Simultaneous blocking of known class A bHLH transcription factors which are expressed in the neural tube by antisense oligonucleotides results in death of differentiating interneurons and has no detectable effect on cell cycle or DNA synthesis in vitro. Blocking the expression of individual class A bHLH transcription factors results no detectable effect. These results demonstrate that GEs are involved in the differentiation of interneurons and have a functional redundancy during neuronal development. Following this study, we established neural plate explant culture from early chick embryo and examine whether neural tube defect occurs or not by blocking their expressions of GEs using antisense oligonucletoides. We added antisense oligonucleotides into single cells by microinjectin. However, neural tube defect did not occur. These experiments suggest that a single gene mutation does not cause neural tube defects.
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