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Growth rate correlates to individual heterozygosity in the European eel, Anguilla anguilla L.
Pujolar, J.M.; Maes, G.E.; Vancoillie, C.; Volckaert, F.A.M.J. (2005). Growth rate correlates to individual heterozygosity in the European eel, Anguilla anguilla L., in: Maes, G.E. Evolutionary consequences of a catadromous life-strategy on the genetic structure of European eel (Anguilla anguilla L.). pp. 161-179
In: Maes, G.E. (2005). Evolutionary consequences of a catadromous life-strategy on the genetic structure of European eel (Anguilla anguilla L.). PhD Thesis. Katholieke Universiteit Leuven. Faculteit Wetenschappen: Leuven. 223 pp., meer
Is gerelateerd aan:
Pujolar, J.M.; Maes, G.E.; Vancoillie, C.; Volckaert, F.A.M.J. (2005). Growth rate correlates to individual heterozygosity in the European eel, Anguilla anguilla L. Evolution 59(1): 189-199. https://dx.doi.org/10.1554/04-377, meer
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Trefwoorden
    Disciplines > Biology > Genetics > Heterozygosity
    Enzymes > Allozymes
    Growth rate
    Microsatellites
    Nucleic compounds > Nucleic acids > Dna > Satellite dna > Microsatellites
    Selection
    Selection
    Marien/Kust
Author keywords
    allozymes; associative overdominance; direct overdominance; growth rate;heterozygosity; microsatellites; selection
Auteurs  Top 
  • Pujolar, J.M.
  • Maes, G.E., meer
  • Vancoillie, C.
  • Volckaert, F.A.M.J., meer
Abstract
    Heterozygosity-fitness correlations (HFCs) have been reported in populations of many species. We provide evidence for a positive correlation between genetic variability and growth rate at 12 allozyme loci in a catadromous marine fish species, the European eel (Anguilla anguilla L.). More heterozygous individuals show a significantly higher length and weight increase and an above average condition index in comparison with more homozygous individuals. To a lesser extent, six microsatellite loci show a similar pattern, with positive but not significant correlations between heterozygosity and growth rate. The HFCs observed could be explained by an effect of either direct allozyme over-dominance or associative overdominance. Selection affecting some of the allozyme loci would explain the greater strength of the HFCs found at allozymes in comparison with microsatellites and the lack of correlation between MLH at allozymes and MLH at microsatellites. Associative overdominance (where allozyme loci are merely acting as neutral markers of closely linked fitness loci) might provide an explanation for the HFCs if we consider that allozyme loci have a higher chance than microsatellites to be in linkage disequilibrium with fitness loci.
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