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Heterosis and the Evolution of Duplications

Janice B. Spofford
The American Naturalist
Vol. 103, No. 932 (Jul. - Aug., 1969), pp. 407-432
Stable URL: http://www.jstor.org/stable/2458991
Page Count: 26
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
Heterosis and the Evolution of Duplications
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Abstract

Single locus heterosis affords a sufficient drive for the incorporation of a newly arisen duplication into a species gene pool. Heterosis is here assumed to result from the formation of heterodimers between polypeptides specified by alleles. In consequence, the normal homologue of the duplication-bearing chromosome is eliminated rapidly unless the product of the locus is regulated in amount and recombination occurs so infrequently as to approximate mutation rates. In the latter case, the duplication comes to a frequency that is the higher, the fewer alleles initially present. This frequency would then continue until the slower processes such as mutation or recombination between adjacent cistrons permit a renewed climb to fixation. The allele included in the duplication will be lost at the original site unless the original number of alleles is low and it forms homozygotes of fitness nearly equal to the heterozygote. In general, segregation would be expected to continue for at least two alleles in nearly equal proportions at the original site. Recombination above a certain minimal value delays the attainment of selective equilibrium. This mechanism would be operative in haploid species as well, although heterosis-maintained segregation would of course not provide either initial or final polymorphism. Although only an arbitrarily simple model was investigated thoroughly, the general conclusions appear unperturbed by various relaxations of the restrictions built into it. Further diversification at the duplication site would be expected to follow its fixation.

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