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Population genetic structure of the African elephant in Uganda based on variation at mitochondrial and nuclear loci: evidence for male-biased gene flow

Authors

  • Silvester Nyakaana,

    1. Zoological Institute, Department of Population Biology, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen Ø, Denmark
    2. Institute of Environment and Natural Resources, Makerere University, PO Box 7298, Kampala, Uganda
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    • Correspondence: S. Nyakaana. Fax: + 256 41 530134; E-mail: muienr@imul.com

  • Peter Arctander

    1. Zoological Institute, Department of Population Biology, University of Copenhagen, Universitetsparken 15, DK-2100 Copenhagen Ø, Denmark
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Abstract

A drastic decline has occurred in the size of the Uganda elephant population in the last 40 years, exacerbated by two main factors; an increase in the size of the human population and poaching for ivory. One of the attendant consequences of such a decline is a reduction in the amount of genetic diversity in the surviving populations due to increased effects of random genetic drift. Information about the amount of genetic variation within and between the remaining populations is vital for their future conservation and management. The genetic structure of the African elephant in Uganda was examined using nucleotide variation of mitochondrial control region sequences and four nuclear microsatellite loci in 72 individuals from three localities. Eleven mitochondrial DNA (mtDNA) haplotypes were observed, nine of which were geographically localized. We found significant genetic differentiation between the three populations at the mitochondrial locus while three out of the four microsatellite loci differentiated KV and QE, one locus differentiated KV and MF and no loci differentiated MF and QE. Expected heterozygosity at the four loci varied between 0.51 and 0.84 while nucleotide diversity at the mitochondrial locus was 1.4%. Incongruent patterns of genetic variation within and between populations were revealed by the two genetic systems, and we have explained these in terms of the differences in the effective population sizes of the two genomes and male-biased gene flow between populations.

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