Bochdanovits Zoltán, Sondervan David, Perillous Sophie, van Beijsterveldt Toos, Boomsma Dorret, Heutink Peter
Section Medical Genomics, Department of Clinical Genetics, Vrije Universiteit Medisch Centrum (VUMC), Amsterdam, The Netherlands.
PLoS One. 2008 Feb 13;3(2):e1593. doi: 10.1371/journal.pone.0001593.
The human genome encodes a limited number of genes yet contributes to individual differences in a vast array of heritable traits. A possible explanation for the capacity our genome to generate this virtually unlimited range of phenotypic variation in complex traits is to assume functional interactions between genes. Therefore we searched two mammalian genomes to identify potential epistatic interactions by looking for co-adapted genes marked by excess two-locus genetic differentiation between populations/lineages using publicly available SNP genotype data. The practical motivation for this effort is to reduce the number of pair-wise tests that need to be performed in genome-wide association studies aimed at detecting GxG interactions, by focusing on pairs predicted to be more likely to jointly affect variation in complex traits. Hence, this approach generates a list of candidate interactions that can be empirically tested. In both the mouse and human data we observed two-locus genetic differentiation in excess of what can be expected from chance alone based on simulations. In an attempt to validate our hypothesis that pairs of genes showing excess genetic divergence represent potential functional interactions, we selected a small set of gene combinations postulated to be interacting based on our analyses and looked for a combined effect of the selected genes on variation in complex traits in both mice and man. In both cases the individual effect of the genes were not significant, instead we observed marginally significant interaction effects. These results show that genome wide searches for gene-gene interactions based on population genetic data are feasible and can generate interesting candidate gene pairs to be further tested for their contribution to phenotypic variation in complex traits.
人类基因组编码的基因数量有限,但却导致了大量可遗传性状的个体差异。对于我们的基因组能够在复杂性状中产生几乎无限范围的表型变异这一能力,一种可能的解释是假设基因之间存在功能相互作用。因此,我们搜索了两个哺乳动物基因组,通过利用公开可用的单核苷酸多态性(SNP)基因型数据,寻找群体/谱系之间由过量两位点遗传分化所标记的共适应基因,以识别潜在的上位性相互作用。这项工作的实际动机是,在旨在检测基因-基因(GxG)相互作用的全基因组关联研究中,通过关注预计更有可能共同影响复杂性状变异的基因对,减少需要进行的成对检验数量。因此,这种方法生成了一份可以进行实证检验的候选相互作用列表。在小鼠和人类数据中,我们都观察到两位点遗传分化超过了基于模拟仅由偶然因素所预期的水平。为了验证我们的假设,即显示过量遗传差异的基因对代表潜在的功能相互作用,我们根据分析选择了一小部分假定相互作用的基因组合,并寻找所选基因对小鼠和人类复杂性状变异的联合效应。在这两种情况下,基因的个体效应并不显著,相反,我们观察到了边缘显著的相互作用效应。这些结果表明,基于群体遗传数据在全基因组范围内搜索基因-基因相互作用是可行的,并且可以产生有趣的候选基因对,有待进一步测试它们对复杂性状表型变异的贡献。