| Project/Area Number | 10358019 |
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 展開研究 |
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| Research Field |
Laboratory animal science
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| Research Institution | Natiomal Institute of Genetics |
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Principal Investigator |
SHIROISHI Toshihiko Natiomal Institute of Genetics, Mammalian Genet Lab, Prof, 系統生物研究センター, 教授 (90171058)
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| Co-Investigator(Kenkyū-buntansha) |
KOIDE Tsuyoshi Natiomal Institute of Genetics,Mammalian Genet Lab,Research Associate, 系統生物研究センター, 助手 (20221955)
若菜 茂晴 財団法人 実験動物中央研究所, 研究プロジェクト推進センター, 室長代理 (90192434)
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| Project Period (FY) |
1998 – 2001
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| Project Status |
Completed(Fiscal Year 2001)
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| Budget Amount *help |
¥41,000,000 (Direct Cost : ¥39,200,000、Indirect Cost : ¥1,800,000)
Fiscal Year 2001 : ¥7,800,000 (Direct Cost : ¥6,000,000、Indirect Cost : ¥1,800,000)
Fiscal Year 2000 : ¥8,000,000 (Direct Cost : ¥8,000,000)
Fiscal Year 1999 : ¥11,700,000 (Direct Cost : ¥11,700,000)
Fiscal Year 1998 : ¥13,500,000 (Direct Cost : ¥13,500,000)
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| Keywords | Chromosome deletion / Japanese wild mouse / chlorambucil / Rapid blood clotting / 精子凍結 / 低血糖傾向 / RLGSマッピング / マイクロサテライトマーカー |
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| Research Abstract |
We carried out in-depth phenotype characterization of mouse mutants identified in screening for chlorambucil (CHL) treated Gl mice. The mutants that we characterized were ; strain ID numbers, CHL0106 and CHL0225. The former mutant showed lower glucose level in serum, and the latter showed rapid blood clotting. Inheritance of these two mutants was confirmed by cross of the mutants with wild-type mice. For the CHL0225, we analyzed platelet coagulation and counted the number of the platelets in order to examine abnormalities of the function and the amount of the platelets. In addition, we assayed activated thromboplastin time, prothrombin time. Moreover, Amount of fibrimonomer complex antithromobin-thromobin complex was measured in order to examine the function of anti-coagulation factors. As a result, we could not find abnormalities in the all parameters of the CHL0225. It indicated that the mutant CHL0225 is not affected in the known coagulation factors, the anti-coagulation factors and the platelet function, but rather unknown gene in the blood clotting cascade is mutated.
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