Deficits of heterozygotes in relation to selective interactions between loci in the mussels brachidontes rostratus and xenostrobus pulex

Abstract

Each marine mussel which has been studied has a polymorphism for leucine aminopeptidase (LAP) loci. In each case, there is a deficit for all, or nearly all, classes of heterozygotes. The consistency of the results suggests that the loci constitute non-transient polymorphisms with heterozygous disadvantage. No satisfactory explanation of this situation has been available. Heterozygous deficits are also often found at other loci in mussels, particularly those encoding aminopeptidase (AP) enzymes. The present work was prompted by the theoretical investigations of Hastings (1982) which revealed the possibility that selective interactions with other loci might enable the maintenance of polymorphisms with marginal underdominance. Non-random associations between genotypes were sought in 10 loci (in four groups of enzymes with related functions) in Brachidontes rostratus and five loci (in two groups) in Xenostrobus pulex. Five of the 30 pairs of loci displayed significant genotypic associations. However, none of these comprised functionally-related enzymes. It remains possible that epistatic interactions may, in special circumstances, be involved in the maintenance of variation. But the process seems unlikely as a general explanation of genotypic frequencies of the LAP and AP polymorphisms of mussels. © The Genetical Society of Great Britain.