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Genome-wide association study of handedness excludes simple genetic models

机译:全基因组关联性研究不包括简单的遗传模型

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Handedness is a human behavioural phenotype that appears to be congenital, and is often assumed to be inherited, but for which the developmental origin and underlying causation(s) have been elusive. Models of the genetic basis of variation in handedness have been proposed that fit different features of the observed resemblance between relatives, but none has been decisively tested or a corresponding causative locus identified. In this study, we applied data from well-characterised individuals studied at the London Twin Research Unit. Analysis of genome-wide SNP data from 3940 twins failed to identify any locus associated with handedness at a genome-wide level of significance. The most straightforward interpretation of our analyses is that they exclude the simplest formulations of the 'right-shift' model of Annett and the 'dextral/chance' model of McManus, although more complex modifications of those models are still compatible with our observations. For polygenic effects, our study is inadequately powered to reliably detect alleles with effect sizes corresponding to an odds ratio of 1.2, but should have good power to detect effects at an odds ratio of 2 or more.
机译:惯用性是一种人类行为表型,似乎是先天性的,通常被认为是遗传的,但其发展起源和潜在因果关系却难以捉摸。已经提出了适合于亲戚之间观察到的相似性的不同特征的惯用性变异的遗传基础模型,但是没有经过果断的测试或确定了相应的致病基因座。在这项研究中,我们应用了在伦敦双子研究室研究的具有良好特征的个体的数据。对来自3940个双胞胎的全基因组SNP数据进行的分析未能在全基因组意义上确定任何与惯性相关的位点。我们分析的最直接解释是,它们排除了Annett的“右移”模型和McManus的“右/机会”模型的最简单表述,尽管这些模型的更复杂的修改仍与我们的观察结果兼容。对于多基因效应,我们的研究不足以可靠地检测具有等于1.2的比值比的效应大小的等位基因,但应具有在2或更高的比值比下检测效应的良好能力。

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