Malaria Journal (Jun 2010)

Population genetic structure of the malaria vector <it>Anopheles nili </it>in sub-Saharan Africa

  • Awono-Ambene Parfait H,
  • Morlais Isabelle,
  • Kengne Pierre,
  • Ayala Diego,
  • Cohuet Anna,
  • Antonio-Nkondjio Christophe,
  • Ndo Cyrille,
  • Couret Daniel,
  • Ngassam Pierre,
  • Fontenille Didier,
  • Simard Frédéric

DOI
https://doi.org/10.1186/1475-2875-9-161
Journal volume & issue
Vol. 9, no. 1
p. 161

Abstract

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Abstract Background Anopheles nili is a widespread efficient vector of human malaria parasites in the humid savannas and forested areas of sub-Saharan Africa. Understanding An. nili population structure and gene flow patterns could be useful for the development of locally-adapted vector control measures. Methods Polymorphism at eleven recently developed microsatelitte markers, and sequence variation in four genes within the 28s rDNA subunit (ITS2 and D3) and mtDNA (COII and ND4) were assessed to explore the level of genetic variability and differentiation among nine populations of An. nili from Senegal, Ivory Coast, Burkina Faso, Nigeria, Cameroon and the Democratic Republic of Congo (DRC). Results All microsatellite loci successfully amplified in all populations, showing high and very similar levels of genetic diversity in populations from West Africa and Cameroon (mean Rs = 8.10-8.88, mean He = 0.805-0.849) and much lower diversity in the Kenge population from DRC (mean Rs = 5.43, mean He = 0.594). Bayesian clustering analysis of microsatellite allelic frequencies revealed two main genetic clusters in the dataset. The first one included only the Kenge population and the second grouped together all other populations. High Fst estimates based on microsatellites (Fst > 0.118, P Conclusion Overall, high genetic homogeneity of the An. nili gene pool was found across its distribution range in West and Central Africa, although demographic events probably resulted in a higher level of genetic isolation in the marginal population of Kenge (DRC). The role of the equatorial forest block as a barrier to gene flow and the implication of such findings for vector control are discussed.