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

The currently known means of formation of haploid sex cells from diploid cells, i.e. meiosis and a number of similar mechanisms known for protozoa, do not include an apparently simpler and the most logical mechanism – simple division of a diploid cell that did not undergo the S-phase after the last division into two haploid cells. For example, during meiosis, the diploid cell is first converted to a cell that is tertraploid from the viewpoint of the amount of genetic material (in S phases of regular cell cycle) and then into four haploid cells through two cell divisions. Similarly, frequently much more complicated processes that initially entail an increase in ploidy and then its reduction are known for a number of groups of protozoa (Reed & Hurst, 1996). Some authors assume that this can be a simple result of and similarly proof that meiosis originally emerged as a mechanism of reduction of polyploidy, which occasionally occurred in cases of defects of synchronization of nuclear and cell division (Cavalier-Smith, 2002). However, this hypothesis does not explain why simplified forms of reduction cell division did not appear secondarily, i.e. after meiosis became a regular part of the cell cycle.A very interesting, although certainly not generally accepted hypothesis – see e.g. (Archetti, 2004), which explains the absence of a mechanism  for the formation of haploid sex cells based on simple division of diploid cells into two haploid cells, assumes that the purpose of the present complicated mechanisms of nuclear division is to prevent the formation and spreading of hypothetical genes termed sister killers (Butcher & Deng, 1994;Hurst, 1993;Haig, 1993). If reduction of ploidy were to occur through simple division of diploid cells into two daughter cells, ideal conditions would be created for the formation and spreading of alleles that, following division of the diploid cells into two haploid cells, would program the haploid cell, in whose nuclei they would be present, to kill its sister haploid cell. The sister-killer allele would, at least initially, spread very rapidly in the population, as heterozygote diploid cells would produce only haploid sex cells with this allele. From the long-term viewpoint, such a system would be unstable

Fig. XII.3 Sister killers.If the gametes are formed by division of diploid cells (a), alleles could be formed and spread in the population that, following division of the maternal diploid cell into two daughter cells, would cause that the gamete with the particular allele would kill its sister cell. If the haploid gamete is formed from a tetraploid cell in a two-step meiosis mechanism, these sister-killer alleles would not be propagated.As it is not possible to determine in advance whether crossing-over occurred (b) or did not occur (c) between the locus containing the given allele, the allele cannot time the killing of the sister cells so as to avoid killing cells containing its own copy. If crossing-over did occur in the given section and the cell kills its sister after the first reduction division, both sister cells will die and the sister-killer allele would not be passed on to the next generation.Sister killing would thus have to be initiated after the second reduction division.However, if crossing-over did not occur in the given section and the cell initiated killing after completion of the second reduction division, both gametes containing the sister-killer allele would kill one another and only the normal alleles would be passed on to the next generation.

as homozygotes with two copies of sister-killer alleles would not produce viable progeny. The allele would have to learn to recognize whether its copy is present in the sister cell and, on this basis, trigger or not trigger killing. Following the creation of such a mechanism, it would become fixed in the given species and would simultaneously cease to be manifested externally in the phenotype. If such a mechanism were not created, the action of sister-killers could even lead to the extinction of the particular species. The third possibility is apparently most probable – through the drastic selection pressure of sister-killer alleles, alleles would become fixed at some locus that would provide their carriers with resistance to sister-killer alleles. Species exposed to constant waves of fixation of sister-killer alleles would, of course, be at a disadvantage compared to species in which a mechanism would exist to prevent the formation of these alleles in advance, so that this mechanism could be fixed in the biosphere by species selection (IV.8.4). Meiosis and other currently known means of creation of haploid sex cells could be the mechanism for preventing the spreading of sister-killer alleles While it is apparent in advance for simple reduction division of heterozygote cells that each of the daughter cells will contain a different allele, this is not true in classical meiosis. Crossing-over occurs at various sites in the individual chromosomes prior to commencement of the first division; during this process, DNA sections are exchanged both between sister chromatids of the same chromosome and also between nonsister chromatids within pairs of homologous chromosomes. As a consequence of these exchanges, two copies of a single allele can be located either on two chromatids of a single chromosome or on the chromatids of two homologous chromosomes. Consequently, it is not possible to decide, in advance, which of the two divisions, of which meiosis consists, entails separation of the two copies of a single allele and which entails the separation of two different alleles (Fig. XII.3). Thus, a sister-killer allele cannot determine whether it should trigger cell killing after the first or second division; in both cases, there is a danger that it will destroy a cell containing its identical copy. Under these circumstances, killing of a sister cell is disadvantageous from the viewpoint both of the individual and of the individual alleles.

We do not currently have any practical proof of the correctness of the hypothesis of the establishment of contemporary meiosis as a defense against the formation of sister-killer alleles and it is not clear how this proof could be obtained. Possibly the only indirect proof is that, in spite of the substantial diversity of various types of reduction division in individual types of organisms, we are not currently aware of a single one that would not simultaneously function as a possible defense against the spreading of sister-killer alleles. Another indirect proof could be the absence of functional genes at sites adjacent to the centromeres. The probability of the occurrence of crossing-over between a certain site and a centromere quite logically decreases with decreasing distance of this site from the centromere. It thus follows that, for genes close to the centromere, even in contemporary two-stage meiosis, the reduction division is almost always the first division, i.e. the division in which homologous chromosomes separate. . Genes located close to the centromere could thus, even now, function as sister-killers and could trigger killing of sister cells after the first meiotic division. The absence of functional genes in the vicinity of the centromere could be a further defensive mechanism of the cell against the formation of sister-killer alleles, or could be a consequence of gradual inactivation of genes that, sometime in the past, acted as sister-killers and thus caused strong selection pressure for the formation of a specific mechanism for their inactivation. In the latter case, the results of genome sequencing projects could provide proof for the correctness of the hypothesis about meiosis as a defense against sister-killer alleles. If it were found that an unusually large number of inactive genes are located in the vicinity of the centromere, e.g. through insertion of a transposon, the hypothesis about the defense against sister-killers would become somewhat more credible and it would be possible to begin to consider experimental verification, e.g. using reactivation of the relevant inactivated gene.