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

In most species whose members can reproduce asexually, the series of asexual reproductions must be interrupted from time to time by sexual reproduction; otherwise the population gradually degenerates, reproduces ever more slowly and finally completely dies out. A single cycle of sexual reproduction is then capable of genetically rejuvenating the particular population, of renewing its reproductive potential and permitting its further existence. A number of authors assume that, during sexual reproduction, some so-far obscure mechanism repairs the mutations and damaged genetic material that have accumulated during the time of asexual reproduction (Bernstein et al. 1985; Avise 1993). If a point mutation occurs in the DNA, in which, for example, one nucleotide is replaced by another nucleotide, the enzymes of the reparation apparatus can find the place where this mutation occurred, as here the bases in the helix do not pair together; however, they cannot determine in which chain a nucleotide exchange occurred. If the cell contains a second copy of the given DNA section, e.g. if a normally haploid organism is passing through its diploid phase during sexual reproduction, the situation is far more favourable. The site where the bases do not pair can be repaired according to the sequence in the second copy of the given DNA section. If DNA replication occurs at the given site without previous reparation of nonpairing bases, the regular DNA structure is renewed and it is then more difficult to recognize the presence of a mutation. However, repair is possible even in this case (see XII.3 and Fig. XII.2). As even neutral mutations can be repaired in this way, this mechanism combined with sexual reproduction appears to be a powerful means of stopping Muller’s ratchet. On the other hand, in a changing environment, the repair of mutations can be disadvantageous in the long term, as it could prevent the particular species from adapting evolutionarily to on-going changes. It is possible that only certain gene sections in the genome could be protected in this way. This possibility is supported, for example, by the results of an in vitro study of the mutagenesis of the gene for DNA polymerase. The results indicated that a number of aminoacid substitutions can be created artificially at a critical site in the enzyme, while the activity or specificity of the mutated enzyme does not change fundamentally and even increases in some cases. Nonetheless, the vast majority of the so-far sequenced DNA polymerases from mutually unrelated organisms have identical or very similar sequences in the given section (Patel & Loeb 2000).

            While the advantageousness of the ability to repair mutations in the germinal line is somewhat doubtful, a similar ability to repair mutations in the somatic cell line is unambiguously advantageous.  According to some authors, diploidy, permitting repair of somatic mutations, is an essential condition for the existence of multicellular organisms (Gorshkov & Makar'eva 1999).