1998 Fiscal Year Final Research Report Summary
Analysis of neural plasticity by transcription factor Otf6
| Project/Area Number |
09680792
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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 |
Neuroscience in general
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| Research Institution | The Institution of Physical and Chemical Research (RIKEN) (1998)
Kyoto University (1997) |
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Principal Investigator |
IKEDA Toshio Riken, Behavioral Genetics, Scientist, 行動遺伝学技術開発チーム, 研究員 (80252526)
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| Co-Investigator(Kenkyū-buntansha) |
ITOHARA Shigeyoshi Behavioral Genetics, Team Leader, 行動遺伝学技術開発チーム, チームリーダー(研究職) (60252524)
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| Project Period (FY) |
1997 – 1998
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| Keywords | transcription factor / embryonic lethal / homologous recombination / knockout mouse / transgenic mouse |
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| Research Abstract |
Mouse lacking the entire Otf6 (Oct-6, Scip, Tst-1) gene locus was generated by homologous recombination in embryonic stem cells. The heterozygous mutants developed normally and were fertile. No homozygous mutant offspring were obtained from intercrosses of heterozygotes, suggesting that this deletion mutation of Otf6 locus was essential for embryonic development. Homozygous mutant embryos died before 8 days post-coitus (dpc). The homozygous mutants were characterized by small size and morphological abnormality compared to the heterozygous mutants and wild types at 7.5 dpc. In addition the BrdU incorporation rate of embryo was reduced in homozygous mutants. In situ labeling for the fragmentation of the genome (TUNEL) suggested that apoptosis occurs in the embryonic cells of homozygous mutant. Consistent with the in vivo results, homozygous mutant manifested growth arrest and rapid death of the inner cell mass in vitro. It has been shown that Mdm2 and Brca1 deficient embryos arrested growth and died at similar embryonic stages. We found that expression of m dm2 but not Brca1 was nearly abolished in homozygous mutant embryos. These results suggest that the developmental arrest of the Otf6 deletion mutants could be caused by the m dm2 pathway.
To analyze the function of Otf6 in adult mouse brain, we produced the conditional gene targeting system using Cre-loxP system and are confirming the specificity of Cre recombinase expression in brain.
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Research Products
(20 results)
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[Publications] Itoh, T., Ikeda T., Gomi, H., Nakao, S., Suzuki, T., Itohara, S.: "Unaltered secretion of beta-amyloid precursor protein in gelatinase A (matrix metalloproteinase 2)-deficient mice"J. Biol Chem.. 272. 22389-22392 (1997)
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「研究成果報告書概要(欧文)」より
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[Publications] Sakaguchi G. Manabe T., Kobayashi, K., Orita S Sasaki T Naito A Maeda M, Igarashi, H., Katsuura. G., Nishioka. H., Mizoguchi, A., Itohara S., Takahashi, t., and Takai, Y.: "Doc2a is an activity-dependent modulator of excitatory synaptic transmission"Eur. J. Neuroscience. 11. 4262-4268 (1999)
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[Publications] Kuwahara C., Takeuchi A. M., Nishimura T., Haraguchi K., Kubosaki A., Matsumoto Y., Saeki K., Matsumoto Y., Yokoyama T., Itohara S., Onodera T.: "Prion protein prevents neuronal cell death"Nature. 400. 225-226 (1999)
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[Publications] Hoq M.M., Suzutani T., Nakaya K., Yoshida I., Ogasawara M., Takeda Y., Shibaki T., Itohara S., Yamamoto H., and Azuma M.: "Insufficient resistance of Trehalose-6,6'-Dimycolate-treated T-cell receptor delta gene mutant (TCRd-/-) mice against influenza virus infection"Microbiol. Immunol.. 43. 491-493 (1999)
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