| Project/Area Number |
01480511
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Laboratory animal science
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| Research Institution | Research Institute for Microbiological Diseases, Osaka University |
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Principal Investigator |
NISHIMUNE Yoshitake Research Institute for Microbiological Diseases, Osaka University Department of Science for Laboratory Animal Experimentation Professor, 微生物病研究所, 教授 (80029793)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥4,600,000 (Direct Cost: ¥4,600,000)
Fiscal Year 1990: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1989: ¥3,400,000 (Direct Cost: ¥3,400,000)
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| Keywords | Differentiation / Cryptorchidism / mutant mouse / animal model / spermatogenesis / germ cell / W gene / Sl gene |
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| Research Abstract |
The effects of Steel-Dickie (Sl^d) mutation and W mutations on testicular germ cell differentiation were investigated using experimental cryptorchidism and its surgical reversal. In Sl^d/+ cryptorchid testes the maintenance of undifferentiated type-A spermatogonia was impaired and their numbers decreased. In contrast, the proliferative activity of type-A spermatogonia in the cryptorchid testis of mutant mice appeared normal as judged by their progression through the cell cycle. Surgical reversal of cryptorchidism resulted in regenerative differentiation of type-A spermatogonia which remained in Sl^d/+ cryptorchid testes was strongly impaired, particularly at two steps of cellular differentiation, from type-A spermatogonia to intermediate or type-B spermatogonia and at meiotic division.
The effect of W, W^f, W^<sh>, and W^v mutations on spermatogenesis in mice was also examined by using experimental cryptorchidism and its surgical reversal. The results indicate that the W gene also exerts its effect on spermatogenic cell differentiation at the same steps as SI gene does. These results of regenerative differentiation of testicular germ cells in both mutant mice indicate that signal transduction between Sl (ligand) and W (c-kit receptor) gene products is important in spermatogenesis of adult mouse.
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