Molecular drive

Molecular drive is a process through which mutations can proliferate within gene families (in process of homogenetization) and within the population (in process of fixation of mutations) through a number of mechanisms of nonreciprocal transfer of genetic information occurring on the chromosome or between different chromosomes (Dover 1986). Molecular drive differs from genetic drift in that changes in the frequencies of the individual alleles that occur through its action are not random in their direction. If a certain population of genetically identical organisms is divided into several smaller populations, then genetic drift will lead to fixation of different alleles in each population. In contrast, the effect of molecular drive should lead to fixation of the same alleles in all populations. Molecular drive differs from selection in that the alleles that are fixed through its action need not favourably affect the phenotype of the organism and can thus have a zero or even negative impact on the biological fitness of the individual. 

In molecular drive, one allele is replaced by another not because this is more advantageous for its bearer, but because, at the level of the DNA, it multiplies more effectively, either through a mechanism related to replication or through a mechanism related to gene conversion (see below).

Molecular drive differs from mutation bias and reparation drive mainly in that it is responsible for the proliferation of certain mutations in the genome or in the gene pool of the population, but not for their repeated formation.

Molecular driveentails a number of mechanisms connected primarily with replication, recombination and repairing of nucleic acids. These mechanisms favour the formation and proliferation of certain sequential motifs in the gene pool of the population regardless of the degree to which the existence of these motifs is manifested in the phenotype of the organism and the degree to which it affects its biological fitness. The best-known processes active in the functioning of molecular drive include gene conversion, transposition, and also processes directly dependent on replication, i.e.uneven crossing-over andslipped-strand mispairing (Tachida 1993).

The existence of molecular drive is most clearly manifested in the evolution of repetitive DNA segments in closely related species (Charlesworth, Sniegowski, & Stephan 1994; Petes & Fink 1982). These segments are frequently located in the genome in a great many copies, of the order of hundreds of thousands. The individual copies are very similar and frequently completely identical. Simultaneously, repetitive sequences in closely related species are very different. It is difficult to explain this phenomenon without postulating the existence of a specific mechanism capable, following the speciation event – after the splitting off of a new species, of causing parallel differentiation in the repetitive DNA segments in all the loci of the genome. As the speciation process can hardly cause or affect the differentiation of repetitive genes, it is more reasonable to assume that this process occurs continuously in the gene pool of each species. Speciation division of the originally uniform gene pool into two gene pools alone only makes this visible, i.e. permits the repetitive sequences in the two gene pools to develop in different directions.

At the present time, it is mostly assumed that a random process of differentiation of repetitive genes occurs continuously in the gene pool of organisms and thus that mutations are accumulated in the individual copies of the repetitive gene. However, the process of homogenization of the individual copies also occurs simultaneously, i.e. a process in which the variants of the repetitive genes that are most successful from the standpoint of replication, transposition or gene conversion proliferate in the genome at the expense of other variants. In sexually reproducing organisms, the process of homogenization exceeds the boundaries of a single genome and the most successful variant of the repetitive sequence gradually proliferates in the whole gene pool. This is certainly a long-term process; however, it is relatively rapid compared to other evolutionary processes (Fig. VI.9). New variants of repetitive sequences become fixed in a substantially shorter time than the interval separating two subsequent speciation events so that, when studying even closely related species, we find that different variants of the repetitive sequence became fixed in each of them.This fact can be utilized in molecular taxonomy – study of repetitive genes enables discrimination amongst representatives of even very closely related species (Grechko et al. 1998)(see also XXIV.3.9).

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The classical Darwinian theory of evolution can explain the evolution of adaptive traits only in asexual organisms. The frozen plasticity theory is much more general: It can also explain the origin and evolution of adaptive traits in both asexual and sexual organisms Read more