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首页> 外文期刊>Genomics >Genetic Dissection of Femur Breaking Strength in a Large Population (MRL/MpJxSJL/J) of F2 Mice: Single QTL Effects, Epistasis, and Pleiotropy.
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Genetic Dissection of Femur Breaking Strength in a Large Population (MRL/MpJxSJL/J) of F2 Mice: Single QTL Effects, Epistasis, and Pleiotropy.

机译：大群F2小鼠股骨断裂强度的遗传解剖（MRL / MpJxSJL / J）：单个QTL效应，上位性和多发性。

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Bone breaking strength is an ultimate measurement of the risk of fracture. For a practical reason, bone mineral density (BMD) has been commonly used for predicting the risk instead. To identify genetic loci influencing femur-breaking strength (FBS), which was measured by three-point bending using an Instron DynaMight Low-Force Testing System, the whole-genome scan was carried out using 119 polymorphic markers in 633 (MRLxSJL) F2 female mice. We identified six significant quantitative trait loci (QTL) affecting bone breaking strength on chromosomes 1, 2, 8, 9, 10, and 17, which together explained 23% of F2 variance. Of those, the QTL on chromosomes 2, 8, and 10 seem to be unique to bone breaking strength, whereas the remaining three QTL are concordant with femur BMD QTL. Genetic analysis suggests that, of these six FBS QTL, three influence BMD, two influence bone quality, and one influences bone size. We detected multiple significant epistatic interactions for FBS, which accounts for half (14.6%) of F2 variance compared with significant single QTL effects. We found evidence that pleiotropic effect might represent a common genetic mechanism to coordinately regulate bone-related phenotypes. Pleiotropic analysis also suggests that our current threshold level for significant QTL may be too high to detect biologically significant QTL with small effect. Together with epistatic interactions, these undetected small QTL could explain 30% of genetic variance that remains unaccounted for in this study (heritability estimate for FBS is 68%). Our findings in single QTL effects, epistasis, and pleiotropy demonstrate that partially overlapped but distinct combinations of genetic loci in MRL/MpJ and SJL/J inbred strains of mice regulate bone strength and bone density. Identification of the genes unique to FBS may have an impact on prediction of osteoporosis in human. (c)2002 Elsevier Science (USA).
机译：骨骼断裂强度是骨折风险的最终度量。出于实际原因，通常使用骨矿物质密度（BMD）来预测风险。为了鉴定影响股骨断裂强度（FBS）的基因位点（使用Instron DynaMight Low-Force测试系统通过三点弯曲测量），在633名（MRLxSJL）F2雌性中使用119个多态性标记进行了全基因组扫描老鼠。我们确定了六个重要的定量性状基因座（QTL），它们影响1、2、8、9、10和17号染色​​体上的断骨强度，这一起解释了F2方差的23％。其中，第2、8和10号染色体上的QTL似乎是唯一的断裂强度，而其余三个QTL与股骨BMD QTL一致。遗传分析表明，在这六个FBS QTL中，三个影响BMD，两个影响骨骼质量，一个影响骨骼大小。我们检测到FBS的多个显着上位相互作用，与显着的单个QTL效应相比，占F2方差的一半（14.6％）。我们发现证据，多效效应可能代表了一个共同的遗传机制，以协调调节骨相关的表型。多向性分析还表明，我们当前的重要QTL阈值水平可能太高而无法检测到生物学上重要的QTL，但影响很小。连同上位相互作用，这些未检测到的小QTL可以解释30％的遗传变异，而该变异在本研究中仍未解决（FBS的遗传力估计为68％）。我们在单个QTL效应，上位性和多效性方面的发现表明，MRL / MpJ和SJL / J自交系小鼠遗传位点的部分重叠但截然不同的组合可调节骨强度和骨密度。 FBS独特基因的鉴定可能对预测人类骨质疏松症有影响。 （c）2002 Elsevier Science（美国）。

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