GENETICS OF GROWTH-RATE VARIATION IN BIVALVES - ANEUPLOIDY AND HETEROZYGOSITY EFFECTS IN A CRASSOSTREA-GIGAS FAMILY

• Published in: Genome
• Main Authors: Thiriotquievreux, C, Pogson, Gh, Zouros, E
• Other Authors: Station Zoologique de Villefranche, Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)
• Format: Article in Journal/Newspaper
• Language: English
• Published: HAL CCSD 1992
• Subjects: [SDU.STU.OC]Sciences of the Universe [physics]/Earth Sciences/Oceanography; Crassostrea gigas; Pacific oyster
• Online Access: https://hal.science/hal-03476518; https://doi.org/10.1139/g92-007

International audience Enzyme homozygosity and somatic aneuploidy are both known to adversely affect juvenile growth rate in marine bivalves. We have examined the joint effects of these two factors by scoring genotypes at nine segregating allozyme loci and counting the numbers of chromosomes lost in 30 cells in each of 83 full sibs of the Pacific oyster. A highly significant negative correlation was observed between the number of chromosomes missing and shell length in full sibs of the same age. No relationship was seen, however, between allozyme heterozygosity and either shell length or chromosome loss, nor was there any difference in the distribution of aneuploidy among genotypes at any given enzyme locus. Thus, the effects of homozygosity and aneuploidy on growth rate appear to have different genetic bases. Even in the most aneuploid oysters, more than half the cells examined had a complete chromosome complement of 2n = 20. This eliminates somatic aneuploidy as an explanation for the excess of enzyme homozygosity frequently observed in populations of marine molluscs. Significant deviations from Mendelian expectations, favoring homozygotes at some loci and heterozygotes at others, were recorded at eight of the nine allozyme loci, but these occurred independently of the aneuploidy observed. Our results suggest that within families a much larger component of variation in growth rate is due to aneuploidy than to allozyme genotype, but this conclusion cannot, at present, be extended to natural populations.