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

An allele that codes an inactive product of the particular gene or that is not even expressed usually acts as recessive. If the second allele on a homologous chromosome codes a functional product, for example, a functional enzyme, then this protein occurs in both a homozygote and in a heterozygote and the result is the presence of the particular trait. The degree of expression of the individual genes is usually substantially regulated by the current need for the particular product in the cell, so that the fact that only single functional copy of a certain gene is present in a heterozygote need not be manifested in the concentration of the product of the given gene. Even if regulation of the expression of the given gene is not possible and the amount of the given product depends on the gene dose, i.e. on the number of functional copies in the nucleus, the reduced concentration of the product in a heterozygote need not be manifested in its phenotype, especially if this product is an enzyme participating in a complicated metabolic process. A greater number of enzymes participate in the individual metabolic pathways in a certain cascading sequence. It simultaneously follows from the laws of enzyme kinetics that the overall rate of subsequent reactions is only slightly sensitive to fluctuations in the concentrations of the individual enzymes (Kacser & Porteous 1987).

If the product of a given gene is not an enzyme but a structural or regulation molecule, a mutated allele can very easily have a dominant character and manifestation. For example, a regulation protein that gains new affinity for a regulation site of a particular gene can turn on the expression of this gene even in the cell of a heterozygote. Such an allele can act as a dominant allele. Similarly, an allele coding an altered form of an alosterically regulated enzyme, i.e. an enzyme whose activity is, for example, inactivated when the products of the reaction that it catalyzes bond to it, can act as a dominant allele. If a mutated allele codes an enzyme that, because of the mutation, has lost the ability to be alosterically inactivated in the presence of the products of the particular reaction, then the presence of such an allele is understandably also manifested in the presence of normal alleles coding the original, regulated enzyme.

Fig. II.11 Selection in favour of dominant and recessive alleles. The effectiveness of selection in favour of dominant alleles, with a low frequency of alleles in the population (q), is much higher than in favour of similar recessive alleles. In the graph, the effectiveness of selection in favour of the individual alleles is expressed as a change in the frequency of the given allele per time unit (dq/dt). In case of dominant alleles, the rate of increase in the frequency of suitable alleles is high even at a low frequency of alleles. This substantially reduces the risk that a new mutated allele will disappear soon after its formation through the effect of drift. Here, both alleles exhibit the same selection coefficient in the homozygote state and differ only in that the presence of recessive alleles does not in any way affect the biological fitness of heterozygotes.

A certain amount of direct and indirect evidence demonstrates that the dominance of alleles is actually a more complex phenomenon that is, itself, the subject of biological evolution (Bourguet 2001). For example, it was repeatedly found that, in the natural population, the most common alleles are usually dominant and, on the other hand, minority alleles are frequently recessive. If, on the other hand, we isolate individuals in the laboratory that bear two newly formed mutated alleles, or if we obtain individuals bearing minority alleles in mutually isolated natural populations, then the relationship of partial dominance is mostly found between their alleles. This fact can be interpreted in two quite different ways. The first explanation is based on the quite logical assumption that suitable dominant alleles will be more readily spread in the population and will thus become majority alleles more readily than similarly advantageous recessive alleles. While the usefulness of dominant alleles is also manifested in a heterozygote, the usefulness of similar recessive alleles is manifested only in recessive homozygotes, in the outbred population, i.e. in a population in which random crossing occurs between its members, i.e. only when its frequency is substantially increased (Fig. II.1). This principle is called Haldane’s sieve (Noor 1999).

The second explanation is based on the assumption that the degree of dominance, like any other biologically important property, can be the subject of natural selection and can thus be the subject of biological evolution. Imagine a gene that simultaneously participates in the formation of two traits, A and B. Simultaneously, its allele a₁ determines the formation of trait A and its allele a₂ determines the formation of trait B. If the presence of trait A is advantageous for the individual and simultaneously the presence of alleles coding the trait B is also advantageous, natural selection can finally lead to one allele being dominant from the standpoint of trait A (and recessive from the standpoint of trait B) and the other allele of the same gene, to the contrary, being recessive from the standpoint of trait A (and dominant from the standpoint of trait B). As a consequence, heterozygotes will benefit from the presence of both trait A and traitB. The generally known fact of the high biological fitness of individuals that are heterozygote in a large number of genes indicates that this could occur very frequently in nature.

The dominance of majority alleles can also be considered to be a manifestation of stabilizing selection, which leads to increased ability, termed developmental canalization, i.e. the ability of an organism to balance and eliminate during its ontogenesis the effects of disturbances following both from unpredictable effects of the external environment, and also genetic effects, e.g. in damage to one of the copies of its genes as a result of mutation (see XII.7.2). It can be expected that an organism that is capable of maintaining an optimal course of its ontogenesis in spite of a wide range of unpredictable effects will be at an advantage in competition with an organism with less robust ontogenesis.