Search

Juveniles of the blue mussel Mytilus edulis that had resulted from a large number of pair matings were examined at six polymorphic enzyme loci. In four loci, the overall number of heterozygotes was significantly less than expected from the parental genotypes. The degree of deviation from expectation varied considerably among families, and families which shared the same male parent tended to show similar degrees of deviation. Inbreeding and population mixture, the two most cited explanations of heterozygote deficiency (a phenomenon commonly observed in populations of marine bivalves), do not apply in the case of pair-matings, and the null allele hypothesis is inconsistent with the data. These observations suggest that genotype-dependent larval mortality constitutes the most probable cause of this phenomenon.

Shell length and electrophoretic heterozygosity at six enzyme loci were scored in juveniles of 30 hatchery-grown families and in adults of 10 field-grown families of the blue mussel Mytilus edulis. A total of 4 809 offspring were scored. We found no consistent pattern in the correlations between shell length and enzyme heterozygosity among sibs within families. However, a significant family effect on shell length was observed, suggesting an influence of background genotype on this character. A family effect on viability was also observed. When the environment and family effects were accounted for, a small positive correlation between heterozygosity and shell length at the juvenile stage remained. This correlation was significant in one of the three experiments. No such correlation was evident at the adult stage. Our interpretation of these results is that electrophoretic alleles appear to have no direct of independent effect of their own on growth. We suggest that the negative correlation of homozygosity with these characters, seen in natural populations, results from homozygosity for hidden recessive deleterious genes with which the electromorphs are in a steady state of quasilinkage disequilibrium.