Frozen Evolution. Or, that’s not the way it is, Mr. Darwin. A Farewell to Selfish Gene.

The mechanism of meiosis should ensure, amongst other things, that the members of a heterogamete sex will produce the same number of gametes with two different sets of sex chromosomes and thus the ratio of males and females in their progeny will equal 1:1. However, for a number of species, populations are known in which the ratio of males and females differs substantially from the theoretical ratio of 1:1. In some cases, meiotic drive is responsible for this deviation (Carvalho & Vaz 1999). Alleles proliferating in the gene pool through the action of this mechanism are denoted as SRD (sex ratio distorters). For example, in the mosquito Aedes aegypti, gene D (distorter), whose active allele causes decomposition of the X-chromosomes in future sperm, is located on the Y-chromosome close to gene M, i.e. the gene that determines male sex. Males with active allele D thus produce far fewer viable sperm, and most of them contain a Y-chromosome and thus lead to the formation of males. The SRD system on the X-chromosome of several species of drosophila acts similarly, but in the opposite direction.

            The distortion of the sex ratio in favour of males (Aedes) or in favour of females (Drosophila) can, of course, seriously affect the existence of the population. According to some authors, in many species this process can substantially affect the behaviour of the entire meta-population, specifically the rate of formation and disappearance of local subpopulations (Carvalho & Vaz 1999).

            Large evolutionary plasticity and the great variety of genetic sex-determining mechanisms is currently explained by the existence of the selection pressure of the SRD-allele, specifically the necessity from time to time of formation of substitute mechanisms capable of compensating the distorted sex ratio that occurs with proliferation of certain SRD alleles (Werren & Beukeboom 1998).