Evolution of a malaria resistance gene in wild primates

Jenny Tung (), Alexander Primus, Andrew J. Bouley, Tonya F. Severson, Susan C. Alberts and Gregory A. Wray
Additional contact information
Jenny Tung: Duke University
Alexander Primus: Duke University
Andrew J. Bouley: Duke University
Tonya F. Severson: Institute for Genome Sciences and Policy, Duke University,
Susan C. Alberts: Duke University
Gregory A. Wray: Duke University

Nature, 2009, vol. 460, issue 7253, 388-391

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.

Date: 2009
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DOI: 10.1038/nature08149

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