The genetic control of 11 electrophoretically detected allozyme polymorphisms in the oyster Crassostrea virginica was investigated in 10 pair crosses. For nine allozyme loci, each offspring shared at least one band (electromorph) with each parent. For the remaining two loci (mannosephosphate isomerase and leucine aminopeptidase-2), some offspring failed to share a band with one or both parents. Several lines of evidence indicated that these anomalous results were due to transmission of null alleles. There was evidence of distorted segregation at 8 of the 11 loci. The departures from the Mendelian expectations within the pair crosses might be due either to viability selection in the offspring or to gametic selection in one or both parents, although the possibility that the distortion is due to a locus linked to the allozyme locus cannot be ruled out. However, there was no evidence that heterozygosity per se had an effect on viability of offspring within a cross. Linkage analysis revealed two linkage groups, one consisting of four allozyme loci and the other consisting of three loci.