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

The hypothesis of revolt of ultraselfish genes is based on the idea that, in the area of the genome in which recombination does not occur, ultraselfish genetic elements can accumulate and spread in the population by one of the mechanisms of evolutionary drive (see Chap. VI). Generally, the cooperation of several genes is required for their spreading, say gene A, whose product would damage the chromosomes derived from the other parent, and gene B, whose products would protect the chromosomes from the same gene set and thus from the same parent, against the action of the product of gene A (Fig. XXI.11). If both genes are located on an autosome, they can be separated in the progeny as a result of genetic recombination, understandably with catastrophic results for spreading of gene A – in the next generation, it will damage the chromosomes of both chromosome sets and thus basically commit genetic suicide. In contrast, the genes in the nonrecombining DNA sections, i.e. particularly in unpaired sex chromosomes (allosomes) Y and W, are always transferred together and thus form a sort of supergene. They can form coalitions and spread in the gene pool of the population even at the expense of the average viability of its members.
The parliament of genes model (Leigh 1972) assumes that the spreading of such ultraselfish genes in the population is very rapidly prevented by the spreading of some other gene, to be precise some alleles of some other gene, which are capable of neutralizing the function of the ultraselfish gene. Genes on chromosome Y can be readily inactivated, for example by integration of a transposon or retrotransposon. This could be connected with observed accumulation of transposons, in humans primarily retrotransposons, in nonrecombining Y-chromosome areas (Erlandsson, Wilson, & Paabo 2000). Within a species, ultraselfish genes that are located on allosomes are not greatly manifested as they are “held in check” by the appropriate neutralizer genes, located on the other chromosomes. However, as soon as an allosome in a hybrid finds itself in the presence of a foreign gene set, the ultraselfish genes can begin to act and damage both the fertility and viability of their bearers (Tao, Hartl, & Laurie 2001). The presence of its own chromosome set with the relevant neutralizer genes need not necessarily protect a hybrid against the action of an ultraselfish gene, as neutralizer genes can, for example, be capable of protecting only their own chromosome. For example, these can be alleles that have lost the target site for the product of the ultraselfish gene. Another possibility is that the neutralizer can act (for example by protecting the target sites on the chromosome of their own chromosome set by methylation) during the progress of gametogenesis, i.e. sooner than the chromosomes in the zygote come into interaction with the products of the ultraselfish gene.
            _{The results of some experiments and a number of observations in nature support the action of ultraselfish genes in the formation of postzygotic interspecific barriers (Orr & Presgraves 2000). It has been found primarily in flora that one of the potential consequences of interspecific hybridization and also, e.g., polyploidization (Wendel 2000) consists in the activation of genetic elements of the transposon type, their cutting out and insertion into new sites (Comai 2000). Compared to animals, plants have a far more dynamic genome and are frequently capable of repairing damage to their DNA occurring as a consequence of increased transposon activity. Reparation is frequently accompanied by fundamental restructuring of the genome and this restructuring can also be substantially manifested in the phenotype of hybrid flora and their progeny. It is probable that the passivity of transposons in normal plants is a result of neutralizer genes that are gradually fixed in the gene pool of the plant as a result of transposone selection pressure. Neutralizer genes need not occur in the genome of a foreign species or their functioning in a genome containing the chromosomes of a foreign species are greatly limited so that they are not capable of completely controlling the transposons activity.}