Establishment of congenic strains of mice carrying a genomic interval which regulates the onset of osteoporotic phenotype.
Project/Area Number |
11470308
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Research Category |
Grant-in-Aid for Scientific Research (B).
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Orthopaedic surgery
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Research Institution | KYOTO UNIVERSITY |
Principal Investigator |
TSUBOYAMA Tadao Kyoto University, College of Medical Technology, Professor, 医療技術短期大学部, 教授 (90261221)
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Co-Investigator(Kenkyū-buntansha) |
HOSOKAWA Masanori Kyoto University, Institute for Frontier Medical Science, Associate Professor, 再生医科学研究所, 助教授 (00127135)
|
Project Period (FY) |
1999 – 2000
|
Project Status |
Completed (Fiscal Year 2000)
|
Budget Amount *help |
¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 2000: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1999: ¥4,200,000 (Direct Cost: ¥4,200,000)
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Keywords | osteoporosis / animal model / genetic background / QTL / SAM / congenic strain / polygene |
Research Abstract |
Previously, we identified two quantitative trait loci (QTLs) specifying the peak relative bone mass on chromosomes (Chrs) 11 and 13 by interval mapping in two mouse strains, SAMP2 and SAMP6. The latter strain is an established murine model of senile osteoporosis and exhibits a significantly lower peak relative bone mass than SAMP2. In this study, we constructed interval-specific congenic strains in order to dissect the polygenic trait into single gene factors. By seven consecutive backcrosses and intercrossmating of the N7mice, four congenic strains (P2.P6-pbd1^a, P2.P6-pbd2^a, P6.P2-pbd1^b, P6.P2-pbd2^b) were produced. P2.P6-pbd1^a and P2.P6-pbd2^a had a SAMP6-derived 48cM interval from Chr 11 and a SAMP6-derived 15cM interval from Chr 13, respectively, on a SAMP2-derived background. To the contrary, P6.P2-pbd1^b and P6.P2-pbd2^b had a SAMP2-derived 32cM interval from Chr 11 and SAMP2-derived 15cM interval from Chr 13, respectively, on a SAMP6-derived background. Microdensitometry, dual-energy X-ray absorptiometry, and peripheral quantitative computed tomography revealed lower bone density in P2.P6-pbd1^a and P2.P6-pbd2^a than in the background SAMP2 mice. These measurements showed lower bone density in P6.P2-pbd1^b and P6.P2-pbd2^b than in the background SAMP6 mice. These results confirmed the existence of loci regulating bone density on Chr 11 and Chr 13 in the SAM stains.
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Report
(3 results)
Research Products
(12 results)