on gene frequency. This occurs because the bottleneck leads to the dispersal of gene frequencies and the reduction in mean heterozygosity, so for the AA model, if frequencies are initially intermediate (e.g. 0.5) there is a substantial increase in V A/V G, whereas if frequencies initially follow the ‘U’ distribution, there is little V AA initially, total variance falls and the level of dispersion and V A/V G do not increase appreciably. Indeed, for a population that starts with the gene frequency distribution U-shaped, the loss of heterozygosity is due to fixation. Among the genes that remain segregating the distribution of gene frequencies flattens considerably, and in the absence of new mutation approaches the uniform distribution which has a lower ratio of V A/V G than the ‘U’ distribution. However, despite this, V AA declines faster than V A because, as loci become fixed, the number of pairs of segregating loci declines faster than the number of segregating loci. Thus it is not obvious what effect the bottlenecks in livestock, laboratory or human populations have had on the ratio V A/V G. We suspect it has not been large because, if a large reduction in heterozygosity had occurred, these populations
