Author:

Keywords:

Anguilla, Animals, Aquaculture, Body Size, Body Weight, Environment, Enzymes, Fish Diseases, Heterozygote, Microsatellite Repeats, Stress, Stress, Psychological, Survival Rate, Variation (Genetics), Science & Technology, Life Sciences & Biomedicine, Biotechnology & Applied Microbiology, Genetics & Heredity, allozymes, European eel, fitness, heterozygosity, microsatellites, ontogeny, stress, survival, SCALLOP PLACOPECTEN-MAGELLANICUS, MULTIPLE-LOCUS HETEROZYGOSITY, GROWTH-RATE, ENZYME HETEROZYGOSITY, GENETIC-VARIATION, ATLANTIC SALMON, ALLOZYME, POPULATION, SELECTION, L., 0604 Genetics, 0703 Crop and Pasture Production, 1001 Agricultural Biotechnology, Plant Biology & Botany, 3105 Genetics

Abstract:

Heterozygosity-fitness correlations (HFCs) have been reported in populations of many species, although HFCs can clearly vary across species, conspecific populations, temporal samples, and sexes. We studied (i) the temporal stability of the association between genetic variation and growth rate (length and mass increase) and (ii) the influence of genetic variability on survival in the European eel (Anguilla anguilla L). HFCs were assessed using genotypes from 10 allozyme and 6 microsatellite markers in 22-month-old experimental individuals. The results were compared with those of a previous study carried out in 12-month-old individuals, in which more heterozygous individuals showed a significantly faster growth rate. In contrast, 22-month-old individuals showed no evidence that genetic variability was correlated with growth rate. Additionally, heterozygous individuals did not show a higher survival rate compared with more homozygous individuals after either handling stress or parasite infection. The decrease in HFCs over time is consistent with the general prediction that differences in growth and survival among individuals are maximal early in life and in our case most likely due to the relaxation of environmental conditions related to population-density effects. Alternatively, the decline in HFCs could be attributed to either ontogenetic variance in gene activity between 12- and 22-month-old individuals or differential mortality leaving only the largest individuals.