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Imprint of Assortative Mating on the Human Genome

By Loic Yengo, Matthew R. Robinson, Matthew C. Keller, Kathryn E Kemper, Yuanhao Yang, Maciej Trzaskowski, Jacob Gratten, Patrick Turley, David Cesarini, Daniel J Benjamin, Naomi R. Wray, Michael E Goddard, Jian Yang, Peter M Visscher

Posted 13 Apr 2018
bioRxiv DOI: 10.1101/300020 (published DOI: 10.1038/s41562-018-0476-3)

Non-random mate-choice with respect to complex traits is widely observed in humans, but whether this reflects true phenotypic assortment, environment (social homogamy) or convergence after choosing a partner is not known. Understanding the causes of mate choice is important, because assortative mating (AM) if based upon heritable traits, has genetic and evolutionary consequences. AM is predicted under Fisher's classical theory1 to induce a signature in the genome at trait-associated loci that can be detected and quantified. Here, we develop and apply a method to quantify AM on a specific trait by estimating the correlation (θ) between genetic predictors of the trait from SNPs on odd versus even chromosomes. We show by theory and simulation that the effect of AM can be distinguished from population stratification. We applied this approach to 32 complex traits and diseases using SNP data from ~400,000 unrelated individuals of European ancestry. We found significant evidence of AM for height (θ=3.2%) and educational attainment (θ=2.7%), both consistent with theoretical predictions. Overall, our results imply that AM involves multiple traits, affects the genomic architecture of loci that are associated with these traits and that the consequence of mate choice can be detected from a random sample of genomes.

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