Fitness differences associated with Pgi SNP genotypes in the Glanville fritillary butterfly (Melitaea cinxia)

Authors

  • L. ORSINI,

    1. Metapopulation Research Group, Department of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
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  • C. W. WHEAT,

    1. Metapopulation Research Group, Department of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
    2. Department of Biology, Penn State University, University Park, PA, USA
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  • C. R. HAAG,

    1. Metapopulation Research Group, Department of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
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  • J. KVIST,

    1. Metapopulation Research Group, Department of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
    2. Institute of Biotechnology, University of Helsinki, Helsinki, Finland
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  • M. J. FRILANDER,

    1. Institute of Biotechnology, University of Helsinki, Helsinki, Finland
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  • I. HANSKI

    1. Metapopulation Research Group, Department of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland
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Dr Luisa Orsini, Laboratory of Aquatic Ecology and Evolutionary Biology, Katholieke Universiteit Leuven, Ch. Deberiotstraat 32, 3000 Leuven, Belgium.
Tel.: +32 16323707; fax: +32 16320771; e-mail: luisa.orsini@bio.kuleuven.be

Abstract

Allozyme variation at the phosphoglucose isomerase (PGI) locus in the Glanville fritillary butterfly (Melitaea cinxia) is associated with variation in flight metabolic rate, dispersal rate, fecundity and local population growth rate. To map allozyme to DNA variation and to survey putative functional variation in genomic DNA, we cloned the coding sequence of Pgi and identified nonsynonymous variable sites that determine the most common allozyme alleles. We show that these single-nucleotide polymorphisms (SNPs) exhibit significant excess of heterozygotes in field-collected population samples as well as in laboratory crosses. This is in contrast to previous results for the same species in which other allozymes and SNPs were in Hardy–Weinberg equilibrium or exhibited an excess of homozygotes. Our results suggest that viability selection favours Pgi heterozygotes. Although this is consistent with direct overdominance at Pgi, we cannot exclude the possibility that heterozygote advantage is caused by the presence of one or more deleterious alleles at linked loci.

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