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. 1991 May;128(1):133–141. doi: 10.1093/genetics/128.1.133

Expression of Overdominance for Specific Activity at the Phosphoglucomutase-2 Locus in the Pacific Oyster, Crassostrea Gigas

G H Pogson 1
PMCID: PMC1204443  PMID: 1829426

Abstract

Environmental and genetic components of specific activity variation at the phosphoglucomutase-2 locus in the Pacific oyster, Crassostrea gigas, were examined to assess the direct role played by this polymorphism in a heterozygosity/growth relationship. Both environmental variables studied, season and intertidal position, exerted highly significant effects on phosphoglucomutase specific activity but no interactions occurred between these factors and Pgm-2 genotype. Highly significant differences were also detected between Pgm-2 genotypes. The three most common heterozygotes (Pgm-2(92/100), Pgm-2(96/100) and Pgm-2(100/104)) consistently expressed greater specific activities than the Pgm-2(92/92), Pgm-2(96/96), Pgm-2(100/100) and Pgm-2(104/104) homozygotes. Overall, the specific activities of heterozygotes for the Pgm-2(100) allele exceeded heterozygotes by 24% and 20% in the mantle and adductor muscle tissues, respectively. Heterozygotes formed between the three less frequent Pgm-2(92), Pgm-2(96) and Pgm-2(104) alleles differed sharply from those possessing the Pgm-2(100) allele in being indistinguishable from homozygotes. The possibility of these patterns arising from the undetected presence of an inactive Pgm-2 allele was examined and found to be inconsistent with all of its predicted effects on the specific activity data. Genuine overdominance was shown to be capable of explaining the specific activities of ten structural locus genotypes, allelic frequency distributions in natural populations, and the maintenance of the enzyme polymorphism in a balanced state. The results provide evidence favoring the overdominance explanation for one locus involved in a heterozygosity/growth relationship and suggest that the reported effects of this locus on adult body weight may have been caused by the greater flux capacities of heterozygotes for the Pgm-2(100) allele.

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Selected References

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