| Project/Area Number |
10480237
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
KATOH Hideki School of Medicine, Hamamatsu University School of Medicine, Associate Professor, 医学部, 助教授 (30142053)
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| Co-Investigator(Kenkyū-buntansha) |
MUGURUMA Kaori Central Inst for Exp Anim, Researcher, 遺伝, 研究員 (50290979)
NISHIKAWA Tetsu School of Medicine, Hamamatsu University School of Medicine, Associate Professor, 医学部, 教務員 (50260584)
TSUJI Atsushi School of Medicine, Hamamatsu University School of Medicine, Associate Professor, 医学部, 助手 (60303559)
ITOH Toshio Central Inst for Exp Anim, Senior Scientist, 動物医学, 室長 (20106644)
EBUKURO Michi Central Inst for Exp Anim, Researcher, 遺伝, 研究員 (40167292)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥7,400,000 (Direct Cost: ¥7,400,000)
Fiscal Year 2000: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1999: ¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 1998: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | Mouse / fsn^<Jic> gene / hypertriglyceridemia / extramedullary hematopoiesis / genetic background / leukemia / pleiotropy / psoriasis / コンジェニック系統 / 戻し交配 / 同座性 / allelism / 変異遺伝子 / 劣性遺伝子 / マイクロサテライトDNA / MSM系統マウス / Flaky skin / 突然変異 / 高脂血症 / 血液生化学的検査 / 致死遺伝子 / 交配実験 / リンケージ(連鎖) |
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| Research Abstract |
We studied a new spontaneouslly occurred mutants arisen in the INT strain, which die around 14 days after birth. In this study, we tried to demonstrate causes of death and chromosomal location of a causing gene. The results are as follows.
1. Hematological studies : Comparing normal mice, the numbers of platelets and white blood cells in the affected mice were increased 1.8 and 1.6 times, respectively. Increase of WBC suggested that the affected mice suffered from leukemia.
2. Biochemical studies : The concentrations of triacylglycerol (triglyceride) and unesterified free fatty acid (FFA) in bloods were increased 7 times and that of free cholesterol 2.5 times comapring those of normal mice. This mutant is a hypertriglyceridemia.
3. Genetic studies : Mapping of the gene causing the various defects was carried out using backcrosses with the MSM strain. The results revealed that the gene is recessive and is mapped at 56cM from centromere of Chr 17. This new mutation was demonstrated to be an allele of the fsn (flaky skin) mutation with phenotypes similar to those of the int mutation. The int mutation was named fsn^<Jic> according to the rules of International Nomenclature Committee of the mouse.
4. Histopathological studies : Massive vacuolation caused by steatosis (fatty degeneration) was observed in livers of the mutant mice. Also, an increase of the number of nucleated cells in livers, kidneys and spleens revealed a possibility of extramedullary hematopoiesis.
The results described above demonstrated that the fsn^<Jic> mutation caused a typical pleiotropy displaying failures in various organs and tissues. In this study, the causal gene was genetically identified, but was not etiologically done.
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