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The evolution of TEP1, an exceptionally polymorphic immunity gene in Anopheles gambiae

Darren J Obbard1, Deborah M Callister1, Francis M Jiggins1, Dinesh C Soares2, Guiyun Yan3 and Tom J Little1*

Author Affiliations

1 Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, West Mains Rd, Edinburgh EH9 3JT, UK

2 School of Chemistry, Joseph Black Building, King's Buildings, University of Edinburgh, Edinburgh EH9 3JJ, UK

3 Program in Public Health, College of Health Sciences, University of California at Irvine, 252 Hewitt Hall, Room 3038, Irvine CA 92697-4050b, USA

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BMC Evolutionary Biology 2008, 8:274  doi:10.1186/1471-2148-8-274

Published: 7 October 2008



Host-parasite coevolution can result in balancing selection, which maintains genetic variation in the susceptibility of hosts to parasites. It has been suggested that variation in a thioester-containing protein called TEP1 (AGAP010815) may alter the ability of Anopheles mosquitoes to transmit Plasmodium parasites, and high divergence between alleles of this gene suggests the possible action of long-term balancing selection. We studied whether TEP1 is a case of an ancient balanced polymorphism in an animal immune system.


We found evidence that the high divergence between TEP1 alleles is the product of genetic exchange between TEP1 and other TEP loci, i.e. gene conversion. Additionally, some TEP1 alleles showed unexpectedly low variability.


The TEP1 gene appears to be a chimera produced from at least two other TEP loci, and the divergence between TEP1 alleles is probably not caused by long-term balancing selection, but is instead due to two independent gene conversion events from one of these other genes. Nevertheless, TEP1 still shows evidence of natural selection, in particular there appears to have been recent changes in the frequency of alleles that has diminished polymorphism within each allelic class. Although the selective force driving this dynamic was not identified, given that susceptibility to Plasmodium parasites is known to be associated with allelic variation in TEP1, these changes in allele frequencies could alter the vectoring capacity of populations.