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Genetic evidence for a higher female migration rate in humans

Nature Genetics 20, 278–280 (1998) | Download Citation

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Abstract

Mitochondrial DNA and the Y chromosome have been used extensively in the study of modern human origins and other phylogenetic questions, but not in the context of their sex-specific modes of transmission. mtDNA is transmitted exclusively by females, whereas the Y chromosome is passed only among males. As a result, differences in the reproductive output or migration rate of males and females will influence the geographic patterns and relative level of genetic diversity on the Y chromosome, autosomes and mtDNA (ref. 1). We have found that Y chromosome variants tend to be more localized geographically than those of mtDNA and the autosomes2,5. The fraction of variation within human populations for Y chromosome single nucleotide polymorphisms (SNPs) is 35.5%, versus 80–85% for the autosomes and mtDNA (refs 6, 7, 8). A higher female than male migration rate (via patrilocality, the tendency for a wife to move into her husband's natal household) explains most of this discrepancy, because diverse Y chromosomes would enter a population at a lower rate than mtDNA or the autosomes. Polygyny may also contribute, but the reduction of variation within populations that we measure for the Y chromosome, relative to the autosomes and mitochondrial DNA, is of such magnitude that differences in the effective population sizes of the sexes alone are insufficient to produce the observation.

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Acknowledgements

We thank all the DNA donors who participated in this project. Laboratory work was funded by NIH grant GM28428 to L.L.C.-S. The collection of DNA samples in Ethiopia, Sudan and Mali was supported by the Arthur Green Fund of Harvard University and the L.S.B. Leakey Foundation, with the assistance of E. Bekele, M. Ibrahim, M. Traoré and A. Touré. M.T.S. was a U.S. National Science Foundation Predoctoral Fellow. We thank M. Feldman for helpful advice and discussion.

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  1. Program for Population Genetics, Harvard School of Public Health, 665 Huntington Avenue, Boston, Massachusetts 02115, USA.

    • Mark T. Seielstad

  2. Department of Genetics, Stanford University School of Medicine, Stanford, California 94305-5120, USA.

    • Eric Minch
    •  & L. Luca Cavalli-Sforza

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Correspondence to Mark T. Seielstad.

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https://doi.org/10.1038/3088

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