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Results for “assortative mating”

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PubMed2026

The paradoxical extinction: Exploring signatures of assortative mating as a possible mechanism that maintains canonical Red Wolf genetic ancestry in the American Gulf Coast canids.

Admixed genomes, particularly those with an evolutionary history of genetic exchange with an endangered or extinct species, are valued for innovative and unconventional conservation actions. Here, we show the substantial conservation value that the admixed canids of the Gulf Coast have as they retain high amounts of contemporary Red Wolf ancestry and unique genetic variation of past Red Wolf lineages (e.g. ghost ancestry). We analyzed 54,439 loci genotyped across the genome of 413 North American canids and investigated the role that assortative mating with respect to ancestry proportions played in the retention of endangered genetic variation. We report high correlations of inter-chromosomal ancestry proportions that varied with geographic location along Texas and Louisiana Gulf Coast populations, with the stronger signatures reported in the latter. We found that models of assortative mating promoted greater ancestry variance compared with random mating leading to increased efficiency of selection for Red Wolf and ghost alleles. Despite the Red Wolf being extinct in the wild, original, and ghost genomic variation persists in Gulf Coast admixed canids. We suggest two conservation strategies that value and preserve this unique and endangered genomic variation through designed breeding programs. Ultimately the incorporation of this ghost genetic variation would be valuable to boost the genetic viability of the ex situ Red Wolf breeding program, create in situ redundancy, and avoid extinction for this endemic American wolf species.

Animals↗
PubMed2014

Genetics and intelligence differences: five special findings.

Intelligence is a core construct in differential psychology and behavioural genetics, and should be so in cognitive neuroscience. It is one of the best predictors of important life outcomes such as education, occupation, mental and physical health and illness, and mortality. Intelligence is one of the most heritable behavioural traits. Here, we highlight five genetic findings that are special to intelligence differences and that have important implications for its genetic architecture and for gene-hunting expeditions. (i) The heritability of intelligence increases from about 20% in infancy to perhaps 80% in later adulthood. (ii) Intelligence captures genetic effects on diverse cognitive and learning abilities, which correlate phenotypically about 0.30 on average but correlate genetically about 0.60 or higher. (iii) Assortative mating is greater for intelligence (spouse correlations ~0.40) than for other behavioural traits such as personality and psychopathology (~0.10) or physical traits such as height and weight (~0.20). Assortative mating pumps additive genetic variance into the population every generation, contributing to the high narrow heritability (additive genetic variance) of intelligence. (iv) Unlike psychiatric disorders, intelligence is normally distributed with a positive end of exceptional performance that is a model for 'positive genetics'. (v) Intelligence is associated with education and social class and broadens the causal perspectives on how these three inter-correlated variables contribute to social mobility, and health, illness and mortality differences. These five findings arose primarily from twin studies. They are being confirmed by the first new quantitative genetic technique in a century-Genome-wide Complex Trait Analysis (GCTA)-which estimates genetic influence using genome-wide genotypes in large samples of unrelated individuals. Comparing GCTA results to the results of twin studies reveals important insights into the genetic architecture of intelligence that are relevant to attempts to narrow the 'missing heritability' gap.

Genetic Predisposition to Disease↗
PubMed2025

Separating direct, indirect and parent-of-origin genetic effects in the human population.

Here, we present a novel approach to estimate the degree to which the phenotypic effect of a DNA locus is attributable to four components: alleles in the child (direct genetic effects), alleles in the mother and the father (indirect genetic effects), or is dependent upon the parent from which it is inherited (parent-of-origin, PofO effects). Applying our model, JODIE, to 30,000 child-mother-father trios with phased DNA information from the Estonian Biobank (EstBB) and the Norwegian Mother, Father, Child Cohort (MoBa), we jointly estimate the phenotypic variance attributable to these four effects unbiased of assortative mating (AM) for height, body mass index (BMI) and childhood educational test score (EA). For all three traits, direct effects make the largest contribution to the genetic effect variance. But we find that parental indirect genetic effects make an equivalent combined contribution, and that there is a non-zero PofO effect variance for all traits. We calculate the heritability that would be obtained at the population-level in the absence of AM for common DNA loci, and show that the proportional contribution of direct effects to these heritability values can be calculated as 64.0% for EA in MoBa, 77.1% and 63.4% for height in MoBa and EstBB, and 81.2% and 88.0% for BMI in MoBa and EstBB. Additionally, using within-family genome-wide association testing, we identify 276 independently associated DNA regions that replicate across two additional biobanks, which all show a genotype-phenotype relationship that reflects an interplay of direct, indirect and PofO effects. Determining how direct, parental and PofO genetic effects combine across loci genome-wide to influence human phenotypic variation requires joint modeling of parental and child genotypes alongside the parental origin of loci and here, we make the first attempt to do this in the human population.

EstBB↗