Plant & Animal Genome VI Conference

W10

SEGREGATION OF ALLOZYMES AND MICROSATELLITES IN INBRED AND OUTBRED PACIFIC OYSTER POPULATIONS.

1. CRC for Aquaculture, CSIRO Division of Marine Research, Castray Esplanade or GPO Box 1538 , Hobart, Tasmania 7001
2. CSIRO Division of Marine Research, Castray Esplanade or GPO Box 1538 , Hobart, Tasmania Au. 7001
3. CSIRO Division of Tropical Agriculture, Level 3, Gerhmann Laboratories, Research Road, St. Lucia, Brisbane, Q Au. 4072

Inbreeding is often viewed in an animal breeding context as the mating of related parents which produces an increased probability of identity of descent among genes in the progeny. If inbreeding has fitness effects in inbred progenies (hence producing inbreeding depression), segregation distortion can result at genetic marker loci due to homozygosity for deleterious or lethal recessive genes and to the loss of interactions among genes. Hard conclusions about the distorted transmission of molecular markers in the Pacific oyster await more statistically powerful inferences from designed experiments. However, it appears as if the magnitude of segregation distortion at microsatellite and allozyme loci is about equal and an increasing function of the inbreeding coefficient. In 50% inbred families, 51% of the 14 allozyme loci distorted. In 25% inbred families 50% of the 6 allozymes distorted and 36% of the 11 microsatellites distorted. In F₂ progenies, who are not themselves inbred but are derived from mating inbred but unrelated parents, distortion was still severe as 60% of 5 allozymes and 54% of the 13 microsatellites distorted. In the progeny of crosses of non-inbred pairs, 20% of 15 microsatellite loci distorted. Layered on top of inbreeding-related distortion of Mendelian segregation ratios due to zygotic selection is the apparently high frequency of null alleles at microsatellite loci in natural populations of the Pacific oyster (which can introduce problems with genotypic classification), and some rare indications of imprinting at microsatellite loci. Three factors ultimately contribute to the distortions; 1) zygotic selection 2) null alleles and 3) imprinting. These distortions appear structured i.e., they occur in clusters of apparently linked loci. Therefore, segregation distortion is presented in reference to the statistical linkage relationships among allozymes, microsatellites and now AFLP markers. AFLP markers do not appear to suffer from segregation distortion in crosses with no history of inbreeding. Inferences are discussed in the context of a statistical linkage map including allozymes, microsatellites and AFLP markers.