Chromosomal regions harboring genes for the work to femur failure in mice

被引:20
作者
Li X. [1 ,2 ]
Masinde G. [1 ,2 ]
Gu W. [1 ,2 ]
Wergedal J. [1 ,2 ]
Hamilton-Ulland M. [1 ,2 ]
Xu S. [1 ,2 ]
Mohan S. [1 ,2 ]
Baylink D.J. [1 ,2 ]
机构
[1] Molecular Genetics Division, Musculoskeletal Disease Center, Loma Linda University, Loma Linda, CA 92357
[2] Department of Botany and Plant Sciences, University of California, Riverside
关键词
Bone mineral density; Instron; Quantitative trait loci; Work to failure;
D O I
10.1007/s10142-001-0045-z
中图分类号
学科分类号
摘要
The work to failure is defined as the maximum energy bone can absorb before breaking, and therefore is a direct test of the risk of fracture. To determine the genetic loci influencing work to failure, we have performed a high density genome-wide scan in 633 (MRL× SJL) F2 female mice. Five loci (P < 0.005) with significant effects on work to failure were found on chromosomes 2, 7, 8, 9, and X, which collectively explained around 20% variance of work to femur failure in F2 mice. Of those, only the QTL on chromosome 9 was concordant with bone mineral density (BMD) QTLs. Eight significant interactions (P < 0.01) between marker loci were identified, which accounted for an equivalent amount of F2 variance (23%) to combined single QTL effects. Our results demonstrate that most of the genetic loci regulating work to failure are different from those for BMD in the 7-week-old female mice. If this is also true in humans, this finding will challenge the predictive value of BMD for the risk of fracture.
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页码:367 / 374
页数:7
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