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HETEROZYGOSITY AND GROWTH IN MARINE BIVALVES: FURTHER DATA AND POSSIBLE EXPLANATIONS
Author(s) -
Zouros E.,
RomeroDorey M.,
Mallet A. L.
Publication year - 1988
Publication title -
evolution
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.84
H-Index - 199
eISSN - 1558-5646
pISSN - 0014-3820
DOI - 10.1111/j.1558-5646.1988.tb04192.x
Subject(s) - loss of heterozygosity , biology , overdominance , gonad , heterozygote advantage , population , genetics , correlation , natural population growth , evolutionary biology , genotype , gene , allele , demography , anatomy , geometry , mathematics , sociology
In a natural population of two‐year‐old mussels, shell length was correlated with degree of heterozygosity. There was no correlation between an individual's glycogen level and its degree of heterozygosity, but when individuals were grouped in heterozygosity classes a near‐significant correlation was observed between degree of heterozygosity and mean glycogen level corrected for the effects of sex and stage of gonad development. There was no correlation between degree of heterozygosity and index of gonad development. Such a correlation would have provided support for the hypothesis (Zouros and Foltz, 1984) that dependence of time of spawning on heterozygosity may explain the observed heterozygote‐deficiency. The causes of heterozygote‐deficiency, a common phenomenon in populations of marine bivalves, remain obscure. The observed heterozygosity‐growth correlation is examined in the light of the controversy of whether allozymes act as markers in linkage association with genetic conditions that are responsible for the differences in growth among individuals or are themselves the agents of the correlation. The observations that 1) the contributions of individual loci to the correlation vary among populations, 2) the correlation is observed in samples from natural populations but not among progeny from pair matings, and 3) the correlation is nearly always accompanied with heterozygote‐deficiency in the population are more compatible with the first explanation and suggest that the growth‐heterozygosity correlation results mostly from associative overdominance and to a lesser extent from the direct contributions of scored loci to growth.