ArticleAmerican journal of human genetics2001
Gene conversion and different population histories may explain the contrast between polymorphism and linkage disequilibrium levels.
Article in American journal of human genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 145 papers.
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145 citing papers in PubMed.
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- Variability and forensic efficiency of 12 X-STR markers in Namibian populations.International journal of legal medicine · 2024Article
- The Linkage-Disequilibrium and Recombinational Landscape in Daphnia pulex.Genome biology and evolution · 2022Article
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- Revisiting the notion of deleterious sweeps.Genetics · 2021Article
- How Good Are Predictions of the Effects of Selective Sweeps on Levels of Neutral Diversity?Genetics · 2020Article
- Footprints of natural selection at the mannose-6-phosphate isomerase locus in barnacles.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Evaluating the quality of the 1000 genomes project data.BMC genomics · 2019Article
- The Effects on Neutral Variability of Recurrent Selective Sweeps and Background Selection.Genetics · 2019Article
- 1000 human genomes carry widespread signatures of GC biased gene conversion.BMC genomics · 2018Article
- How strong was the bottleneck associated to the peopling of the Americas? New insights from multilocus sequence data.Genetics and molecular biology · 2018Article
- Comparison of Single Genome and Allele Frequency Data Reveals Discordant Demographic Histories.G3 (Bethesda, Md.) · 2017Article
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- Biased gene conversion skews allele frequencies in human populations, increasing the disease burden of recessive alleles.American journal of human genetics · 2014Article
85 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
To characterize linkage disequilibrium (LD) levels in human populations, we have analyzed 10 independent noncoding segments in three population samples from the major ethnic groups--that is, Africans, Asians, and Europeans. Descriptive statistics show that LD decays much faster in the African samples than in the non-African ones. With the assumption of an equilibrium model, we estimated the population crossing-over parameter (4N(e)r(bp), where N(e) is the effective population size and r(bp) is the crossing-over rate per generation between adjacent base pairs) in the presence of gene conversion. In the African sample, LD and polymorphism levels lead to similar estimates of effective population size, as expected under an equilibrium model. Conversely, in both non-African samples, LD levels suggest a smaller effective population size than that implied by polymorphism levels. This observation is paralleled by significant departures from an equilibrium model in the spectrum of allele frequencies of the non-African samples. Besides ruling out the possibility that non-African populations are at equilibrium, these results suggest different demographic history (temporal and spatial) of these groups. Interestingly, the African sample fits the expectations of an equilibrium model based on polymorphism and divergence levels and on frequency spectrum. For this sample, the estimated ratio of gene conversion to crossing-over rates is 7.3 for a mean tract length of 500 bp, suggesting that gene conversion may be more frequent than previously thought. These findings imply that disease-association studies will require a much denser map of polymorphic sites in African than in non-African populations.
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