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Evolution of a malaria resistance gene in wild primates

Author

Listed:
  • Jenny Tung

    (Duke University
    Institute for Genome Sciences and Policy, Duke University,)

  • Alexander Primus

    (Duke University
    Institute for Genome Sciences and Policy, Duke University,)

  • Andrew J. Bouley

    (Duke University)

  • Tonya F. Severson

    (Institute for Genome Sciences and Policy, Duke University,)

  • Susan C. Alberts

    (Duke University
    Institute for Genome Sciences and Policy, Duke University,
    Duke University, Durham, North Carolina 27708, USA
    Institute of Primate Research, National Museums of Kenya)

  • Gregory A. Wray

    (Duke University
    Institute for Genome Sciences and Policy, Duke University,
    Duke University, Durham, North Carolina 27708, USA)

Abstract

Shared resistance to malaria In humans, variation in the FY gene, also called DARC, can make the difference between susceptibility or resistance to infection by the malaria parasite Plasmodium vivax. FY codes for a chemokine receptor on the surface of red blood cells that is a known entry point for the malarial parasite. Now a study of a population of yellow baboons in Amboseli National Park in Kenya has identified variation in the FY gene of the baboon as a key determinant of susceptibility to the malaria-like parasite Hepatocystis. The functional variants in the baboon FY gene are not homologous to those seen in humans, though the patterns of variation in the FY cis-regulatory gene region in baboons and human raise the possibility of both mechanistic and selective parallels between the two species.

Suggested Citation

  • Jenny Tung & Alexander Primus & Andrew J. Bouley & Tonya F. Severson & Susan C. Alberts & Gregory A. Wray, 2009. "Evolution of a malaria resistance gene in wild primates," Nature, Nature, vol. 460(7253), pages 388-391, July.
    • Handle: RePEc:nat:nature:v:460:y:2009:i:7253:d:10.1038_nature08149
    DOI: 10.1038/nature08149
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