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The Biological Bulletin, Vol 188, Issue 2 117-119, Copyright © 1995 by Marine Biological Laboratory
RESEARCH NOTES |
J. E. Toro and A. M. Vergara
Instituto de Biologia Marina, Universidad Austral de Chile, Casilla 567, Valdivia, Chile
Reports of heterozygote deficiencies in electrophoretic surveys carried out in marine bivalves abound in the literature (1-6) but the mechanism or mechanisms producing this phenomenon have not been well defined. We report that, in the Chilean oyster (Ostrea chilensis), heterozygote deficiencies in a cohort obtained by mass spawning in the laboratory are not randomly distributed in time among genotypes. The eggs of the Chilean oyster are internally fertilized, and the larvae, which are brooded within the mantle cavity, have limited dispersal capabilities because of their extremely short pelagic stage (7). These features could allow mechanisms such as inbreeding or Wahlund effect to produce heterozygote deficiencies. However, we observed no significant heterozygote deficiencies in juveniles at 6 months of age; instead allozyme heterozygosity decreased over time. Inbreeding, Wahlund effect, aneuploidy, and null alleles are unlikely to be main causes of the heterozygosity deficiency in this cohort; if they were, the deficiency should be evident from the juvenile stage and would not necessarily increase over time (2, 5, 8, 9, 10). We suggest that selection against heterozygotes is the most probable cause of the increasing degree of heterozygote deficiency with age in this cohort of O. chilensis, a proposition that accords with data for other marine bivalve species (2, 4, 11).
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