Heterozygote Deficiencies and Allozyme-Associated Heterosis in Marine Bivalves

自然群体的遗传变异调查 海洋生物，特别是双壳类， 悖论：许多基因显示出杂合子的缺陷， 根据人口遗传理论预期的频率，然而， 同时，杂合子个体似乎享受增强的 成长和生存。 造成这种情况的原因只能是 通过受控实验室实验来理解。 在这个项目中，超过一百个家庭的白腹蛤蜊， Mulinia lateralis，将在实验室生产和饲养。 通过比较父母和后代的基因型， 家庭的一系列基因，研究人员将能够 确定数量不足的原因，并加强 杂合子适合度 一个潜在的来源是自发的 染色体畸变（非整倍体）的同一类型，导致 很大一部分的人类出生缺陷。 如果这被证明 在这种情况下，海洋双壳类可能成为有价值的模型系统， 用于非整倍体的研究。 或者，如果适应性 差异可归因于生物化学差异， 基因产物，这一发现将进一步帮助我们了解 自然界中遗传变异进化意义 人口。

Surveys of genetic variation in natural populations of marine organisms, particularly bivalves, have revealed a curious paradox: many genes show a deficiency of heterozygotes compared to frequencies expected under population genetic theory, yet at the same time heterozygous individuals appear to enjoy enhanced growth and survival. The reasons for this situation can only be understood by controlled laboratory experiments. In this project, over a hundred families of the coot clam, Mulinia lateralis, will be produced and reared in the laboratory. By comparing the genotypes of the parents and offspring in each family for a series of genes, the investigators will be able to determine the origin(s) of the numerical deficiency and enhanced fitness of heterozygote. One potential source is spontaneous chromosomal aberrations (aneuploidy) of the same type that cause a large proportion of birth defects in humans. If this proves to be the case, marine bivalves could become valuable model systems for the study of aneuploidy. Alternatively, if the fitness differences are attributable to biochemical differences in the gene products, this finding will further aid our understanding of the evolutionary significance of genetic variation in natural populations.