Structured mating: Patterns and implications

Sebro, Ronnie; Peloso, Gina M.; Dupuis, Josée; Risch, Neil

doi:10.1371/journal.pgen.1006655

Cited by 29 publications

(37 citation statements)

References 43 publications

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“…When looking at the genome-wide pattern of relatedness among spouses, we found a signal of similarity between spouses in all samples except the UK and Spain. Such a pattern complements previous observations [2] and may result from the tendency to mate with someone from the same location or neighbourhood [66,67] (likely to be genetically closer than a more distant individual [68,69]), or from the tendency to mate with a distant cousin [9]. Alternatively, such a pattern may be generated under random mating if the data were collected from different geographical areas and then aggregated for the analysis.…”

Section: Discussionsupporting

confidence: 72%

Genomic evidence for MHC disassortative mating in humans

et al. 2019

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Although pervasive in many animal species, the evidence for major histocompatibility complex (MHC) disassortative mating in humans remains inconsistent across studies. Here, to revisit this issue, we analyse dense genotype data for 883 European and Middle Eastern couples. To distinguish MHC-specific effects from socio-cultural confounders, the pattern of relatedness between spouses in the MHC region is compared to the rest of the genome. Couples from Israel exhibit no significant pattern of relatedness across the MHC region, whereas across the genome, they are more similar than random pairs of individuals, which may reflect social homogamy and/or cousin marriages. On the other hand, couples from The Netherlands and more generally from Northern Europe are significantly more MHC-dissimilar than random pairs of individuals, and this pattern of dissimilarity is extreme when compared with the rest of the genome. Our findings support the hypothesis that the MHC influences mate choice in humans in a context-dependent way: MHC-driven preferences may exist in all populations but, in some populations, social constraints over mate choice may reduce the ability of individuals to rely on such biological cues when choosing their mates.

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Section: Discussionsupporting

confidence: 72%

Genomic evidence for MHC disassortative mating in humans

et al. 2019

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“…Assortative mating, differently from high level of inbreeding that affects the frequency of all loci independently, is a phenotype-based assortative mating (driven by different factors such as educational level, socioeconomic status, language, behaviour, culture etc.) and can change LD and the distribution of the genotype frequencies of the loci involved in the assortment to an excess of homozigosity 92 . Accordingly a recent study showed that genetic variants linked to education predict longevity, suggesting that individuals with more education-linked genetic variants had longer-living parents 93 .…”

Section: Familial Ecology and The Genetic Of Longevitymentioning

confidence: 99%

Genetics of Human Longevity Within an Eco-Evolutionary Nature-Nurture Framework

2018

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Genetics of human longevity within an eco-evolutionary nature-nurture framework. -Circulation Research 2018 ; 123(7) : 745-772.The final published version is available online at: https://www.ahajournals.org/ ABSTRACTHuman longevity is a complex trait, and to disentangle its basis has a great theoretical and practical consequence for biomedicine. The genetics of human longevity is still poorly understood, despite a number of investigations that used different strategies and protocols. Here we argue that such rather disappointing harvest is largely due to the extraordinary complexity of the longevity phenotype in humans. The capability to reach the extreme decades of human lifespan appears to be the result of an intriguing mixture of geneenvironment interactions. Accordingly, the genetics of human longevity is here described as a highly context-dependent phenomenon, within a new integrated, ecological and evolutionary perspective, and is presented as a dynamic process, both historically and individually. The available literature has been scrutinized within this perspective, paying particular attention to factors (sex, individual biography, family, population ancestry, social structure, economic status and education, among others) that have been relatively neglected. The strength and limitations of the most powerful and used tools, such as GWAS and whole-genome sequencing, have been discussed, focusing on prominently emerged genes and regions, such as APOE, FOXO3, IL-6, IGF-1, chromosome 9p21, 5q33.3 and somatic mutations among others. The major results of this approach suggest that: i) the genetics of longevity is highly population-specific; ii) small-effect alleles, pleiotropy and the "complex allele timing" likely play a major role; iii) genetic risk factors are age-specific and need to be integrated in the light of the geroscience perspective; iv) a close relationship between genetics of longevity and genetics of age-related diseases (especially cardiovascular diseases) do exist. Finally, the urgent need of a global approach to the largely unexplored interactions between the three genetics of human body, i.e. nuclear, mitochondrial and microbiomes, is stressed. We surmise that the comprehensive approach here presented will help in increasing the above-mentioned harvest.

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“…Previous studies 18–20 have been successful at detecting GPD by direct quantification of increased homozygosity at ancestry-associated loci. Beyond ancestry-related traits, such endeavour is particularly challenging for polygenic traits as theory 14 predicts an increase of homozygosity due to AM inversely proportional to the number M of causal variants 14,21 .…”

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confidence: 99%

“…negligible ( Supplementary Note 1 ). Extremely large studies would therefore be required to quantify systematic deviation from HWE at height-associated single-nucleotide polymorphism (SNP) as shown in a recent study 18 that failed to detect such an effect. Another study 23 in ∼6,800 participants of European ancestry, reported evidence of deviation from HWE at height associated loci.…”

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confidence: 99%

“…This study however did not account for within-sample population stratification and therefore their reported estimates are likely inflated for this reason. Overall, study designs using deviation from HWE for quantifying GPD can be successful for detecting ancestry-based AM (ancestral endogamy) because the number of loci distinguishing ancestries is relatively small 24 , and ancestral endogamy is strong 18 , but are less powerful to detect trait-specific AM. In contrast to HWE-based estimation strategies, quantifying GPD on the basis of pairwise correlations between TIAs is much more tractable as the number of pairs of loci involved, of the order of ∼ M 2 , compensates for the magnitude of the expected covariance for each pair, ∼1/2 M .…”

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confidence: 99%

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Imprint of Assortative Mating on the Human Genome

Yengo

Robinson

Kemper

et al. 2018

Preprint

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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.. CC-BY-NC-ND 4.0 International license It is made available under a (which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.The copyright holder for this preprint . http://dx.doi.org/10.1101/300020 doi: bioRxiv preprint first posted online Apr. 13, 2018; 3 Non-random mating in natural populations has short and long-term evolutionary consequences. In many species, including humans, mate choice is often associated with phenotypic similarities between mates 2,3 . Such phenotypic similarities have multiple sources, for example social homogamy, the preference for a mate from the same environment, or because of primary assortment on certain traits observable at the time of mate choice. Contrary to social homogamy, primary phenotypic assortment, here referred to as assortative mating (AM), has genetic and evolutionary consequences and therefore is the focus of our study. In humans, AM involves multiple complex traits 4-8 and can sometimes lead to similar susceptibility to diseases [9][10][11][12] . The genetic effects of AM were first studied in the seminal articles of Fisher (1918) 1 and Wright (1921) 13 . Those two founding contributions, further complemented by Crow & Kimura (1970) 14 and others [15][16][17] have set the basis of the theory of AM on complex traits. AM theory predicts three main genetic consequences of a positive correlation between the phenotypes of mates in a population: (i) an increase of the genetic variance in the population, (ii) an increase in the correlation between relatives and (iii) an increase of homozygosity (deviation from HardyWeinberg Equilibrium; HWE), in particular at causal loci. These seemingly distinct c...

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Structured mating: Patterns and implications

Cited by 29 publications

References 43 publications

Genomic evidence for MHC disassortative mating in humans

Genomic evidence for MHC disassortative mating in humans

Genetics of Human Longevity Within an Eco-Evolutionary Nature-Nurture Framework

Imprint of Assortative Mating on the Human Genome

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