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

–see Infrapopulation of parasites

see dominance hypothesis

Most of the males in the population can die without any detriment to the reproductive potential of the population. The relatively “cheap price” of male individuals allows males and females to divide some evolutionary roles between them. Females usually take on the function of a conservative agent, whose role lies in transferring tried-and-true traits acquired during evolution from one generation to the next, while males can act as cheap experimental material on which nature can “try out” evolutionary novelties.

            Experimental data related to various animal species indicate that the intraspecies variability of males is usually much greater than the intraspecies variability of females. Similar differences also exist in the death rates as a consequence of congenital deformities in embryos and adult individuals of the male and female sex. This phenomenon can be caused by epigenetic mechanisms valid during ontogenesis. However, in most cases, experimental results have unambiguously demonstrated that a greater number of mutations occur in males than in females. It has, for example, been found that, of 33 new mutations in the gene responsible for the formation of retinoblastoma, 31 were located on the chromosomes derived from fathers and only 2 on chromosomes derived from mothers (Kato et al. 1994). The actual mechanism causing elevated frequency of mutations in males is currently not known; however, this could be connected with the increased number of cell divisions occurring in the formation of male sex cells compared to the number of divisions occurring during the formation of female sex cells (Chang & Li 1995; Drost & Lee 1995; Lessells 1997). However, it can also be imagined that the male organism can, for example, turn off some processes of DNA reparation in the germinal line (Huttley et al. 2000).

Intuition suggests that only structures and mechanisms that represent some kind of selection advantage for their carriers can emerge in evolution (an advantage for the individual, for the population or for the particular species). However, this impression is erroneous. There are a number of situations in which organisms exhibit properties that are clearly detrimental for their carriers, providing an advantage for someone else at his expense. This fact forms the basis for hypotheses about the emergence of sexual reproduction as a manifestation of a selfish gene or as a manifestation of a parasite (Hickey 1993; Bell 1993).

            The idea that one of the most obvious (and most pleasant) patterns of behaviour of contemporary organisms, sexual reproduction, could be a manifestation of the activity of a selfish gene or even a parasite is somewhat surprising. However, the unusualness of an idea is not an argument for or against the validity of a scientific hypothesis._s

During the evolution of any genome, genes could most probably be formed that would cause that their carriers exchanged genetic material with other organisms. While other genes were capable of spreading in the population only vertically in asexually reproducing organisms, i.e. from parents to offspring, through DNA replication, these mutated genes could also spread horizontally, i.e. from one individual to another (Hickey 1993; Bell 1993). One of the ways consists in transfer of a cytoplasmatic genetic agent, plasmid or virus with the relevant gene at the moment of physical contact of two cells. For example, during ciliate conjugation during exchange of nuclei between protozoa, the transfer of an infectious agent can occur very easily. A further type of horizontal spreading of a gene programming sexual reproduction is based on transfer of the gene from one chromosome to another within a single zygote by, for example gene conversion accompanying crossing-overs. The ability to force cells to reproduce sexually and thus create a precondition for horizontal spreading in the population is certainly advantageous for such a gene. It is thus probable that genes with this ability will be evolutionarily very successful and will be readily fixed by natural selection. It simultaneously makes no difference to the gene whether the actual process of sexual reproduction is or is not selectionally advantageous for the particular organism. Genes act selfishly; those that program their carriers so that they are themselves spread most effectively in the population are successful in evolution.

The F-plasmid of bacteria can serve as a prototype for such emergence of a sexual process. This plasmid contains genes encoding the formation of a sex pilus, through which bacteria containing an F-plasmid attach to another bacterial cell and the genes ensure transfer of a copy of the F-plasmid by this pilus to the cells of the recipient. Because the plasmid is capable of integrating into the bacterial DNA or is capable of integrating part of this DNA into itself, it can cause the transfer of bacterial genes during its transfer from cell to cell. Thus, it can be considered to be an adaptive structure that facilitates sexual reproduction for the bacterial cell. Similarly, however, the F-plasmid can be considered to be an infectious agent, a kind of bacteriophage, that has learned not to damage its host cell and that “doesn’t want anything else” than its own reproduction and spreading in the bacterial population. Integration into the bacterial DNA and transfer of bacterial genes thus can constitute only secondary improvement of the effectiveness of the process of plasmid reproduction. A plasmid that integrates into itself, for example, a gene for resistance to antibiotics (R-plasmid) or that is capable of being useful for the bacterial cell in some other way is, of course, at a substantial selection advantage compared to the original F-plasmid.

In the typical case, a mass extinction event is accompanied by a substantial reduction in biodiversity, very frequently not only on a local, but also on a global scale. The individual ecosystems degrade substantially and only a few species remain, which were originally rare before the mass extinction event but subsequently relatively abundant. For example, the beginning of the Mesozoic was characterized by an enormous expansion of stromatolites, while the beginning of the Tertiary witnessed an enormous increase in Foraminifera of the Guembelitria group (Erwin 1998). Many of these species tend to be characterized by small body dimensions – this phenomenon has been described as the Lilliputian phenomenon. These pioneer species are apparently capable of utilizing the degraded environment effectively but are not capable of surviving in competition with other species under normal conditions. Thus, they are a sort of macro-evolutionary analogy of ecological r-strategists. However, in contrast to r-strategists, they apparently did not adapt evolutionarily to the conditions prevailing after mass extinction, but their adaptation, to be more exact exaptation, occurred accidentally or as preadaptation through the action of different selection pressures.
            Over a longer period of time, some of the original species that avoided extinction in locally limited refuges reappear in ecosystems. Of course, some species completely die out and completely disappear from the paleontological record. Some species reappear in the biotope only after a very long time, during which the paleontological record did not contain any traces of them. These species are termed Lazarian species. In contrast to Lazarus of the Bible, we do not know who and why they were called back to life; however, the results of radioactive dating indicate that the personal intervention of Jesus Christ can most certainly be excluded. Cases of “living fossils”, i.e. evolutionarily ancient species or lines that are known in recent fauna and flora and that simultaneously did not occur for long periods of time in the paleontological record, nonetheless indicate that, in some cases species (to be more exact evolutionary lines of subsequent species) can survive tens or even hundreds of million years in geographically or ecologically narrowly defined refuges without leaving any traces in the fossil record.  
            A less fortunate category of species consists in those that also survived a mass extinction, but then died without any successors after its end, usually at the time when the original biodiversity was renewed (Jablonski 2001). These need not be only individual species, but can even correspond to whole higher taxa which, in addition, could have undergone speciation at the normal rate before the beginning of the mass extinction. This is a quite common and striking phenomenon and has been termed “dead clade walking” by paleontologists, an analogy of the 1995 film Dead Man Walking (Jablonski 2002). Once again, it is not apparent why species or higher taxa that prospered in the period prior to a mass extinction and were capable of even surviving through the mass extinction finally succumbed without successors in the subsequent period. It is quite possible that this mass extinction was survived only by those species that were relatively resistant compared to the other species in the taxon but, for some reason, had a reduced rate of speciation.

The individual periods of mass extinction also differ in their degree of specificity, i.e. range of species that are primarily affected. Taxonomic specificity is generally rather low. The members of various developmental lines that live in a similar environment and have similar ecological requirements tend to be affected to the same degree (Raup 1994) (Fig. XXII.7). Nonetheless, it seems that, at least in some cases, a certain taxonomic specificity is manifested For example, mass extinction at the boundary between the Mesozoic and Tertiary affected mainly dinosaurs on the continents, while mammals crossed this boundary with substantially smaller losses. A study performed on 117 North American genera of mammals, reptiles, amphibians and fish demonstrated that 43% of genera became extinct at the end of the Cretaceous. Simultaneously, however, all 22 genera of dinosaurs became extinct, while only 8 of 24 genera of mammals died out. Similarly, only 4 of 12 genera of amphibians became extinct (Raup 1994).
Ecological specificity is usually somewhat greater. Certain communities of organisms were especially affected during some periods of mass extinction, for example communities of marine or, on the other hand, terrestrial ecosystems (Benton 1995). In some cases, on the basis of affecting of the individual types of organisms, it was possible to estimate what was the immediate cause of extinction of organisms in a particular period.

The irregular occurrence of natural catastrophes of various intensities and various geographic extents is a highly probable cause of a substantial number of the episodes of mass extinction. A natural catastrophe is considered to correspond to a change in the environment to which the local organisms are not evolutionarily adapted and that occurs so suddenly or is so radical that the organisms are not capable of evolutionarily adapting to the new conditions. The catastrophe can be of biotic or abiotic origin. In the former case, the cause of the catastrophe could lie in the arrival of a foreign invasive species that uses up or destroys the resources of the local species, or the disappearance of a key species whose presence is essential for the maintenance and proper functioning of the local ecosystems. In the latter case, the cause in the catastrophe could lie in a permanent increase in the water level and flooding of terrestrial ecosystems or a decrease in the water level, destroying the species-rich ecosystems of the continental shelf (Hallam 1989; Raup 1986), a decrease in the oxygen content in a global ocean (Isozaki 1997; Rampino 1996), the eruption of a volcano or the impact of a large cosmic body accompanied by mechanical and thermal destruction of ecosystems, frequently over an extensive area (Renne et al. 1995; Alvarez et al. 1984).
A number of other theoretically possible causes for mass extinction have also been proposed, for example a sudden increase in radioactivity or electromagnetic radiation, caused either by the explosion of a supernova close to the solar system (Ellis & Schramm 1995), or the temporary disappearance of the Earth’s magnetic field that, under normal conditions, blocks the action of cosmic radiation in the surface of the Earth (Loper, McCartney, & Buzyna 1988; Raup 1985). Mass extinctions were apparently connected with the complete or almost complete freezing of the surface of the global oceans to a depth of possibly one kilometer, which most probably occurred at least twice in the Late Precambrian (850 – 590 million years ago) and apparently several times in the Early and Middle Precambrian (the Snowball Earth hypothesis) (Hoffman et al. 1998). The reason for the freezing of the Earth was apparently primarily a slight decrease in the intensity of solar radiation and the secondary existence of positive feedback consisting in greater reflectance of radiation from the frozen surface. No fossils remain from the period of the frozen Earth that would help us to evaluate the effect of this phenomenon on biodiversity; however, the results of physical measurements confirm that almost all photosynthesis disappeared at that time and only bacteria and some anaerobic protozoa could live in the anoxic environment under the ice. However, the results of molecular phylogenetics indicate that the Metazoic divergence is apparently older and it is thus very probable that a suitable refuge must have existed somewhere even in the periods of the frozen Earth, allowing some of the species to survive and to expand to the rest of the territory after melting of the oceans (Runnegar 2000; Hyde et al. 2000)
            In general, it is necessary to recall that the individual causes of mass extinction are not mutually exclusive but, to the contrary, direct causal connections could exist between them. The impact of a cosmic body can initiate flood volcanism, volcanism can (in fact must) cause changes in the atmosphere and subsequently in the climate, changes in the climate can cause both a variation in the sea level and glaciation, where glaciation can subsequently lead to a decrease in the oxygen content in the ocean. Thus, the immediate cause of extinction can be an entirely different phenomenon than that which originally caused the catastrophe.

If the relevant paleontological data are not available or do not permit us to draw unambiguous conclusions and if approaches based on comparison of the ontogeneses of the given forms of the trait similarly fail, we can attempt to differentiate homology and homoplasy on the basis of the maximum parsimony principle. The maximum parsimony principle as employed in phylogenetics states that that the most probable course of cladogenesis is the one that can explain the distribution of the individual forms of traits within the phylogenetic tree through the smallest number of anagenetic changes, i.e. smallest number of transitions from one form of the trait to another. Thus, in looking for the maximally parsimonious tree (Fig. XXIII.5), first all the conceivable trees are created for the studied species, on which the studied species form only the terminal branches, where the form of the trait carried is drawn in next to each species. For all the hypothetical ancestors, i.e. for the inner branches of the tree, the most probable forms of the individual traits are also estimated. The most probable combination of forms of traits for the hypothetical ancestor is then chosen so that the total number of evolutionary changes cable of explaining the distribution of traits in the real studied specie sis as small as possible. If, for example, sister species 1 and 2 carry the trait in form A, then it will be assumed that this form of the trait was also carried by their common ancestor. For each created tree, the number of evolutionary changes in all the traits required to explain the distribution of the individual forms of the traits in the studied species and the tree with the smallest number of necessary changes, i.e. the maximally parsimonious tree, will be considered to be the most probable scheme of cladogenesis for the given phylogenetic line. For a small number of species and small number of traits, the maximally parsimonious tree can be sought for “manually”; however, in the vast majority of cases, a sufficiently powerful computer must be used to solve this task.
            The topology of the resultant tree corresponds to the distribution of most of the traits, i.e. minimizes the overall number of changes in all the traits together, but is usually in contradiction with the distribution of some traits. Traits whose distribution corresponds to the topology are probably homologies. On the other hand, traits whose distribution is contrary to this topology, i.e. traits whose distribution would best suit some other topology, are most probably homoplasies.
            In reconstruction of cladogenesis on the basis of the maximum parsimony principle, we simultaneously form hypotheses about phylogenesis on the basis of hypotheses as to what is a homoplasy and what is a homology and formulate hypotheses on division of traits into homologies and homoplasies on the basis of our hypothesis about the phylogeny of a particular taxon. Thus, there is a danger that, while the created hypotheses will be compatible, both the differentiation of homologies and the reconstruction of phylogenesis will be erroneous. If the obtained phylogram assumes substantially fewer evolutionary changes than the phylograms of other topologies, it is highly probable that it is correct. If the differences between phylograms are not very great in this aspect, it is not possible to rely on the obtained results and it is necessary to obtain new data or use a different method for their processing.
 

see History of evolutionism - neo-Darwinist period

The individual variants of genes (alleles) compete together in biological evolution as to which
will be successfully transmitted to further generations. In cultural evolution, the individual meme variants compete similarly. However, in this case, the competition is not limited only to transmission to the next generation, but also includes effective spreading within a single generation. The meme that is copied (imitated) most often by the members of the population or the members of other species will be most successful. There are various reasons why some memes are imitated more frequently than other memes. Frequently, those memes that are advantageous for their host, bring it some benefit, are copied. However, this is far from being the only reason. Some memes spread because they are easier to copy than other memes, and others because their carriers frequently have a dominant position in the group and the behavior of dominant individuals is usually preferentially copied (Benskin et al. 2002)(Fig. XVII.6). Some memes preferentially spread because they enforce their spreading by some specific mechanisms. For example, the meme for destruction of heathens, either through physical liquidation or conversion to the faith will probably spread faster than the meme for religious tolerance. Analogously, the meme prohibiting the believers of some religions to use contraception will also be successful (Kirk et al. 2001). In the latter case, the effectiveness of the spreading of the particular religion is ensured by cooperation between memes and genes. The carriers of the relevant meme have more children than the carrier of other memes and these children will, with great probability, also inherit the relevant meme from their parents.s

The Darwinian model of biological evolution is characterized by the fact that new useful phenotype traits, to be more precise new alleles, which determine their formation, are formed only by random mutations during evolution. In contrast, an important feature of cultural evolution is that a new meme variant can also be formed as a consequence of targeted, i.e. the purposefully directed activities of an individual.
Ethological experiments on a number of animals have unambiguously demonstrated that individuals faced with a problem, for example the necessity of reaching food that is too high to reach, begin to purposefully look for a suitable way of resolving the particular problem. Simultaneously, they need not progress only by the method of trial and error, but can combine previous experience in dealing with a similar situation. Although the method of trial and error is, for many species, a basic method of creating a great many useful patterns of behavior, the members of some species can employ insight in such a situation. For example, if an experimental chimpanzee could not reach a banana that was suspended high up and was also not even able to knock it down with a stick or by throwing various objects at it, it thought the problem over and, after some time, moved a box under the banana, climbed up on it and picked the banana (Lorenz et al. 1974). Once a successful solution has been found to the particular problem, this is very frequently preferentially adopted by the other animals in the population. Thus, cultural evolution can take place, not only by the mechanism of Darwinian evolution, but also by the mechanism of Lamarkian evolution, i.e. preferential emergence of useful (adaptive) memes and preferential inheritance of just these useful memes.

Some memes can spread very effectively even though they are disadvantageous for their bearers. The meme for smoking spreads in spite of the fact that smoking demonstrably shortens life expectancy and worsens the health of its bearer and persons living in his vicinity, i.e. most frequently his biological relatives, and thus reduces his inclusive fitness (Kunzle et al. 2003; Munafo et al. 2002). The success of the meme for smoking is not only a result of its physiological addiction and the fact that it is imitated by adolescents as a symbol or maturity (and the maintenance of the smoking habit in adulthood is then ensured by the already-mentioned addiction). Smoking, similar to the consumption of chocolate or hard drugs, is pleasant for the individual, at least initially or at the time of consumption. The memes that an individual will attempt to adopt are decided, not by the degree to which they increase or decrease his fitness but by the degree to which they increase his feeling of pleasure or reduce feelings of stress (see XV.2). Even such obviously disadvantageous behavior as suicide, or behavior disadvantageous for its bearer but advantageous for his surroundings, such as some patterns of altruistic behavior, tends to be imitated. Because cultural evolution occurs incomparably faster than biological evolution, there is very little hope that selection against genes that are biologically disadvantageous, i.e. genes determining that biologically disadvantageous behavior will be perceived as unpleasant, could make a species immune to spreading of the particular disadvantageous memes. For example, it cannot be expected that the bad habit of smoking or over-eating sweets would, in time, be reduced by natural selection in that the individuals that find these bad habits pleasant would gradually disappear from the population because they would produce fewer offspring on an average.
            In general, the same rules apply to the spreading of memes as to the spreading of infectious diseases and the relevant processes can also be described by the same formal models (Anderson 1993). The most important parameter that determines the efficiency with which a meme will spread is its basic reproduction constant R0, a dimensionless constant equal to the average number of individuals “infected” by the relevant meme by one bearer of the particular meme in the “naive” population, i.e. a population whose members had not previously encountered the meme. If this constant is larger than 1, the given gene can spread in the population and be retained in it for a long time, even if it is harmful to its bearers, i.e. if it reduces their fitness. The actual reproduction constant, R, in a population in which a certain fraction of individuals, q, was “infected” by the meme in the past, is understandably lower and decreases linearly with increasing fraction of infected individuals. If R decreases to a value of 1, the fraction of infected individuals remains constant in the population and the particular meme is retained endemically in the population. Each meme is differently “infectious” and each has a different threshold intensity, NT, i.e. number of susceptible individuals, at which it can begin to spread in the population. A simple equation exists between the threshold density and R0 
 
      (1)
 
where N is the size of the population. If “meme infection” has occurred in the population, the value of R0 can be calculated from the fraction of individuals that remained unaffected by the meme (s), as it holds that
 
     (2)
 
On the basis of R0 we can then easily calculate the size of the fraction of persons in the population that it would be required to make immune to the particular meme through an effective campaign so that this meme would not be able to spread by horizontal transmission.
 
   (3)
 
If, for example, a certain meme affects an average of 70% of individuals during its natural horizontal spreading in the population, then it would be necessary to “immunize” 41% of the so-far unaffected population in advance to prevent a future meme epidemic. Because the fraction of immunized persons gradually decreases in a natural way after the end of the epidemic, either through the deaths of immune individuals or forgetting, some meme epidemics can have a regular cyclic character, where the periodicity of the cycle will depend on the size of the population.
            Some other interesting laws, which have already been described for classical epidemiology, also govern the spreading of memes (Ewald 1994), see also the chapter XIX.5. Memes (similar to parasites) transmitted exclusively or predominantly vertically, i.e. from parents to children, generally do not harm their bearers, as their successful spreading is closely connected with the fitness of their bearers. In contrast, memes that can spread horizontally can be far more harmful for their bearers. This is especially true of memes that are not transmitted horizontally by direct personal contact between neighbors, but tend to be transmitted over long distances, in the modern world, for example, through the press and television, and are simultaneously not bound to a particular culture, so that they can spread transculturally. Especially harmful memes can spread in populations whose members have a reduced life expectancy for some reason, for example as a result of a war, poor nutrition or diseases. The positive feedback effect can also be important here, where the spreading of the harmful meme reduces the life expectancy of the members of the population, enabling effective spreading of even more harmful memes. The gradual reduction in the occurrence of all possible forms of individual or mass aggression during the second half of the 20th century can be most readily explained as a side effect of the prolonged life expectancy of human beings. The longer this life expectancy, either as a consequence of improved hygiene or advances in medicine, the greater are the penalties for memes that might be successful in the short run, but harm their bearers in the longer term.
The harmfulness of memes is further increased by the possibility of “superinfection”, i.e. increased probability of simultaneous infection of a single person by several memes. If this possibility is negligibly small, an advantage is usually given to those memes that allow their hosts to live as long as possible, so that they are capable of “infecting” a large number of other individuals in the population. However if, during infection by one meme, there is a danger of infection by another meme, even memes that harm their bearers very rapidly can be successful, for example the meme for use of hard drugs. Mutability of memes acts similarly to superinfection. From this point of view, for example, religious systems based on canonized texts will probably be less harmful to their adherents than the religious systems of various sects. Population growth is a factor that can promote the spreading of dangerous memes; memes that are beneficial for their bearers tend to spread in populations with stable sizes or those that are diminishing in size.s

A number of memes are transmitted in the population entirely or primarily from parents to offspring, i.e. via the same direction pathway as genes. As a consequence, together with the successful meme, i.e. with a meme that increases the inclusive fitness of its bearer, the genes that the bearers of the particular gene have in their genome can also spread in the population. However, this can happen only if the bearers of the relevant meme do not reproduce with individuals that do not carry the particular meme. This is generally a rather difficult condition to fulfill, so that ideally this situation can probably occur only for the spreading of the already mentioned meme for killing heathens. However, for a certain structure of the population and means of transmitting memes and genes, the progress of biological evolution can also be affected by cultural evolution when the bearers of the various memes reproduce together. In studies of the genetic polymorphism in four types of cetaceans, it was, for example, found that the mitochondrial DNA of each of the species is practically identical in the entire area (Whitehead 1998; Whitehead 1999).  Similar to most other species of animals, here also the mitochondrial DNA is inherited only from the mother and is practically not subject to genetic recombination. From the viewpoint of population structure, these were matrilinear species in all cases, i.e. species in which the offspring remain in the original herd, while adult males visit other herds for short periods for the purpose of mating. As a result of this type of population structure, memes will also be inherited in the same way as mitochondrial DNA, i.e. down the maternal line. It is known that very intense cultural evolution occurs in cetaceans and the individual herds differ substantially, for example, in the means of obtaining food; the members of a single species catch completely different food in various areas and use very different hunting techniques (Rendell & Whitehead 2001). In some cases, vary rapid spreading of a new pattern of behavior has been observed, for example new hunting techniques within the entire area of occurrence of a particular species (Fig. XVII.7). The authors of the relevant molecular biological studies assume that the  particular mitochondrial DNA variant spreads together with the spreading of the biologically successful meme, i.e. the meme increasing the fitness of its bearer, and that it finally replaced all the other variants in the gene pool of the species.

see History of evolutionism - neo-Darwinist period

Meiosis is a process that should theoretically ensure that homologous chromosomes from the original diploid chromosome set of maternal cells enter the haploid chromosome set of sex cells entirely at random regardless of the alleles that the individual chromosomes contain. However, in actual fact, this is frequently not true and the structure and gene content of the individual chromosomes frequently affect which of the pair of homologous chromosomes finally ends up in the sex cells and which does not. The process of differential transfer of genes to the sex cells through differential transfer of the individual chromosomes is called meoitic drive (Zimmering, Sandler, & Nicoletti 1970; Prout, Bundgaard, & Bryant 1973; Thomson & Feldman 1974).In most cases, meoitic drive occurs during meiosis; however, in some cases, the relevant processes already occur during mitosis, which precedes meiosis or, to the contrary, follows it. To the present day, a number of processes that lead to the origin of meiotic drive have been described.

Meiotic drive occurs very frequently in egg formation. During this process, only one haploid set of chromosomes ends up in the nucleus of the female gamete, while the remaining three sets are eliminated into the polar bodies. In heterozygote females, it very frequently occurs that the probability with which a certain allele will end up in the nucleus of the oocyte or in the polar body, i.e. the probability with which the allele will be transferred to the next generation, differ considerably (Fig. VI.10). (Crow 1979). In some cases a certain allele of a specific gene is proliferated in this way in the population while, in a different case, this can be a certain chromosome mutation (Ruvinsky 1995). If, for example, a laboratory mouse is crossed with a wild house mouse, whose karyotype contains a metacentric chromosome formed through Robertson translocation, i.e. fusion of two acrocentric chromosomes, it has been observed in five cases out of ten that the metacentric chromosome occurs in less than 50% of the progeny of heterozygote females. In some cases, the ratio of the two types of oocyte was as much as 3:1. The authors assumed that the metacentric chromosome would most probably end up in the primary polar body. In another study, monitoring the behaviour of a metacentric chromosome in a population of wild mice, it was observed, on the other hand, that the metacentric chromosome had the greatest probability of ending up in the nucleus of the oocyte (King 1993).

Similar phenomena were also observed for other organisms. For example, it has been observed in sorrel (Rumex acetosa) that only four of nine randomly selected chromosome mutations of the reciprocal translocation type or mutations externally manifested as a shift in centromers exhibited normal Mendelian heredity. In the remaining five, meoitic drive appeared to some degree, in the female or the male plants.

DNA sequencing in the area of the centromere (the site of attachment of microtubules of meiotic spindle and therefore probably an important battlefield for meiotic distorters) in closely related species indicated that these areas are subject to very rapid evolution. It is highly probable that this is the result of a battle between genetic elements proliferating through meoitic drive. According to some authors, a significant part of the DNA in the area around the centromere is formed of these active or inactive elements – meiotic distorters. The predominance of nonsynonymous mutations in the histones that are bonded to the DNA in the area of the centromere, is interpreted in a similar way (a battle between meiotic distorters).Meiotic drive occurs very frequently in egg formation. During this process, only one haploid set of chromosomes ends up in the nucleus of the female gamete, while the remaining three sets are eliminated into the polar bodies. In heterozygote females, it very frequently occurs that the probability with which a certain allele will end up in the nucleus of the oocyte or in the polar body, i.e. the probability with which the allele will be transferred to the next generation, differ considerably (Fig. VI.10). (Crow 1979). In some cases a certain allele of a specific gene is proliferated in this way in the population while, in a different case, this can be a certain chromosome mutation (Ruvinsky 1995). If, for example, a laboratory mouse is crossed with a wild house mouse, whose karyotype contains a metacentric chromosome formed through Robertson translocation, i.e. fusion of two acrocentric chromosomes, it has been observed in five cases out of ten that the metacentric chromosome occurs in less than 50% of the progeny of heterozygote females. In some cases, the ratio of the two types of oocyte was as much as 3:1. The authors assumed that the metacentric chromosome would most probably end up in the primary polar body. In another study, monitoring the behaviour of a metacentric chromosome in a population of wild mice, it was observed, on the other hand, that the metacentric chromosome had the greatest probability of ending up in the nucleus of the oocyte (King 1993).

Similar phenomena were also observed for other organisms. For example, it has been observed in sorrel (Rumex acetosa) that only four of nine randomly selected chromosome mutations of the reciprocal translocation type or mutations externally manifested as a shift in centromers exhibited normal Mendelian heredity. In the remaining five, meoitic drive appeared to some degree, in the female or the male plants.

DNA sequencing in the area of the centromere (the site of attachment of microtubules of meiotic spindle and therefore probably an important battlefield for meiotic distorters) in closely related species indicated that these areas are subject to very rapid evolution. It is highly probable that this is the result of a battle between genetic elements proliferating through meoitic drive. According to some authors, a significant part of the DNA in the area around the centromere is formed of these active or inactive elements – meiotic distorters. The predominance of nonsynonymous mutations in the histones that are bonded to the DNA in the area of the centromere, is interpreted in a similar way (a battle between meiotic distorters).

Another way in which an allele can spread through meoitic drive consists in programming the chromosome that carries the alternative allele to destroy or damage the gamete in which it will end up after the completion of meoisis. This mechanism occurs, e.g. in known systems in the fruit fly Drosophila melanogaster (segregation distortion, SD-systém) and in the house mouse Mus musculus (t-haplotype) (Carvalho & Vaz 1999; Ardlie 1998; Vanboven et al. 1996) (Fig. IV.11). In both cases, meiotic drive occurs during sperm formation and, in both cases, this leads to a smaller number of viable sperm in the ejaculate of a heterozygote male and, in both cases, most of the viable sperm contain the allele that causes this effect. Simultaneously, the destruction of the sex cells containing the normal allele is an active process from the standpoint of the normal allele. If the relevant chromosome does not contain the normal allele in the relevant locus because of deletion, the sperm is not destroyed. This means that the allele responsible for meiotic drive somehow manages to reprogram the normal allele so that, after completion of cell division, it actively damages the spermatid or sperm, in which the nucleus is located. However, it is a certain simplification to speak of an allele in this case; in actual fact, the relevant “allele” consists of a combination of several genes in closely adjacent loci.

The mechanism of meiosis should ensure, amongst other things, that the members of a heterogamete sex will produce the same number of gametes with two different sets of sex chromosomes and thus the ratio of males and females in their progeny will equal 1:1. However, for a number of species, populations are known in which the ratio of males and females differs substantially from the theoretical ratio of 1:1. In some cases, meiotic drive is responsible for this deviation (Carvalho & Vaz 1999). Alleles proliferating in the gene pool through the action of this mechanism are denoted as SRD (sex ratio distorters). For example, in the mosquito Aedes aegypti, gene D (distorter), whose active allele causes decomposition of the X-chromosomes in future sperm, is located on the Y-chromosome close to gene M, i.e. the gene that determines male sex. Males with active allele D thus produce far fewer viable sperm, and most of them contain a Y-chromosome and thus lead to the formation of males. The SRD system on the X-chromosome of several species of drosophila acts similarly, but in the opposite direction.

The distortion of the sex ratio in favour of males (Aedes) or in favour of females (Drosophila) can, of course, seriously affect the existence of the population. According to some authors, in many species this process can substantially affect the behaviour of the entire meta-population, specifically the rate of formation and disappearance of local subpopulations (Carvalho & Vaz 1999).

Large evolutionary plasticity and the great variety of genetic sex-determining mechanisms is currently explained by the existence of the selection pressure of the SRD-allele, specifically the necessity from time to time of formation of substitute mechanisms capable of compensating the distorted sex ratio that occurs with proliferation of certain SRD alleles (Werren & Beukeboom 1998).

It has been estimated that more than 90% of speciation events are accompanied by the formation of a modified karyotype in a daughter species (White 1978). It is probable that, in the case of allopatric speciation, meiotic drive is responsible for this phenomenon or, to be more exact, the fact that the karyotype of the species changes much faster through the effect of meiotic drive than new species are formed. Speciation events only conserve differences in the gene pool of the two populations existing at the given instant and simultaneously create a barrier capable of preventing spreading of chromosome mutations from one population to another. Thus, the karyotypes of two daughter species can diverge. As this divergence occurs through the effect of relatively fast meiotic drive, divergence of karyotypes occurs faster than divergence of phenotypes, which change through the action of the slower processes of genetic drift and selection.

However, in the case of sympatric speciation, it is assumed that meiotic drive could sometimes participate directly in the creation of species barriers and that it could thus actively contribute to the origin of new species. If Robertsonian translocations gradually spread from various areas in the  area occupied by a given species, this entire area can disintegrate into a number of separate areas, where individuals of a different chromosomal race will live in each of them. The boundaries between these areas can be very sharp, especially if two races are next to one another, whose karyotypes contain two different Robertsonian translocations, in which the same acrocentric chromosome, as one of the pair of fused chromosomes, is present (see Fig. XXI.12). Because of the common branch, the two different metacentric chromosomes participate in creation of a chromosome tetrade during meiosis in  hybrids between the two races. Subsequently, disorders occur in the transfer of the chromosomes to the fields of the meiotic spindle and a substantial percentage of nonfunctional gametes is formed. In species in which more intense sperm competition occurs, because the female is often rapidly fertilized by several males in succession, the amount and quality of the sperm in the ejaculate or spermatheca decide the paternity of the individual embryos to a substantial degree. In this case, the heterozygote sons of a male that penetrated into the area of occurrence of a different chromosomal race have substantially reduced biological fitness. This can form a relatively effective barrier against spreading of metacentric chromosomes from the area of one chromosome race into the area of another. Because of the existence of crossing-over, such a barrier need not prevent the flux of the individual genes (or, to be more exact, alleles) between sympatric or parapatric (adjacent) populations of the two chromosome races.  However, reduced fertility of heterozygotes can create very strong selection pressure for the formation of specific recognition mechanisms, capable of preventing mutual crossing of the members of two different chromosome races. If the genes affecting this recognition occur in the area of chromosomes in which crossing-over does not occur for some reason, for example, in the inversion area, it is highly probable that meiotic drive will lead to the formation of two separate species.

Some authors (Ridley 2000)are of the opinion that meiotic drive is an extremely important evolution factor, where the effect of this factor on the average biological fitness of the members of the population is almost always negative. Meiotic drive could be manifested especially strongly in organisms in which crossing-over would not exist and in which alleles would thus not be mixed in pairs of homologous chromosomes. Competition of the individual chromosomes for the most effective spreading in the gene pool of the population through meiotic drive in these cases could generally predominate over competition between the individual alleles for the most effective transfer to further generations through the positive effect on the biological fitness of their bearers, i.e. over natural selection. Crossing-over, which breaks up alliances of alleles of individual chromosomes, is a very effective mechanism limiting the action of meiotic drive, and its development in evolution may even be a necessary condition for the existence of sexual reproduction based on meiosis and syngamy (Haig & Grafen 1991).

Each species has a particular geographic range. Within that range, it exists in individual populations, some of which can be neighbours in terms of space while, on the other hand, others can be more or less isolated. Some populations are permanent, some gradually appear and disappear and some re-locate in space both in the long and in the short term, depending on how the natural conditions evolve in time. Members of these populations interact, including reproduction, mostly within their own population, less frequently with the members of the neighboring populations and least frequently with the members of the most distant populations. However, in many species, an even subtler structure can be discerned within each population, leading to the formation of subpopulations of individuals that are most likely to breed amongst themselves. These subpopulations are usually called demes. Thus, species tend to have a rather complex hierarchical structure, culminating in a metapopulation, i.e. the largest population unit whose members still share a common gene pool and can exchange genes with populations in their range via migrants, and a deme at the other end, whose adult members are most likely to breed amongst themselves. 

Metapopulations differ in both the intensity and the nature of migration occurring between their subpopulations. In some metapopulations, the likelihood of migrant exchange between two subpopulations does not depend on their relative distances, while in others migrants are exchanged primarily between neighboring subpopulations (Fig. VII.1). Migration sometimes occurs along a specific line, such as a coastline, or it can spread in two dimensions, together with the gene flow, covering an area. In the latter case, the rate at which, for example, a mutant allele spreads is substantially lower. Very frequently, one subpopulation produces a large number of migrants covering just a short distance, for example extending only to the neighboring subpopulations and, at the same time, a smaller number of migrants migrating over long distances. Theoretical analyses show that a quite small number of long-distance migrants is sufficient to bring the behaviour of a given system close to that of a system in which elements can interact over any distance. The large effect of a small number of long-distance migrants or a small number of individuals communicating with a large number of other individuals in the system is called the small-world network effect and the processes occurring in these systems are important, for example, in epidemiology (Lloyd & May 2001; Liljeros et al. 2001). Migration between subpopulations tends to be very asymmetrical; some populations produce many migrants, while others produce few but accept large numbers of foreign migrants. As migration often involves exclusively or at least primarily the members of just one sex or gamete (or gametophyte), such as pollen, the intensity of the gene flow on the autosomes, sex chromosomes and in the organelle DNA often varies. The nature of evolutionary processes is different in a metapopulation where the gene flow occurs between more or less permanent subpopulations and a metapopulation where subpopulations constantly disappear and the migrants themselves cause new ones to appear (see VII.8.2) (Shanahan 1998).

see Parasites

In many species, the production of migrants is a costly investment that may not seem very efficient. Many migrants die without offspring, many reach locations that are less favourable in terms of chances for survival. Hamilton (Hamilton & May 1977; Comins, Hamilton, & May 1980) (Fig. VII.2) suggested reasons why many species nevertheless invest a large part of their reproduction potential into producing migrants.  By moving farther away from their parents, migrants reduce the chance of offspring competing with their own family. This situation is extremely beneficial from the point of view of individual inclusive fitness. Thus, an allele “programming” its bearer to produce primarily migrants will be preferred in interallelic competition over an allele reducing the number of migrants produced in favour of production of non-migrant offspring. Another advantage of investing in migrants lies in the fact that migrants have a non-zero chance of reaching an unoccupied location and also in the exponential rise of the newly established population producing more offspring in subsequent generations than the non-migrating individuals under the possibly better conditions in the territory of the parent sub-population, which, however, is already occupied by the species.   

One of the possible explanations of long-term survival of sexuality in the population is based on the same principle. The relevant model, which we will term the Mills of God model, was first described in detail by J. Maynard Smith (Maynard Smith 1993); however, he attributed authorship to M. Williams and G. Price. According to this model, the newly emerging parthenogenetic mutant originally has twice the fitness of its sexually reproducing competitor. However, wedging out the competitor took many dozens of generations in a large population. During this time, the traits of the members of the parthenogenetic clone did not change much, because the only source of its microevolutionary variability consists in rare mutations. In contrast, a population of sexually reproducing individuals permanently generates genetic variability and thus basically exhibits greater microevolutionary plasticity. Consequently, suitable adaptations are formed in time, allowing it to wedge out the parthenogenetic clone.

see Point mutations in the protein-encoding DNA

see Lamarckian microevolution in organisms without Weismann barrier

see Selfish gene theory

Part of neutral mutations is usually gradually fixed in the gene pool of a particular biological species through genetic drift. As the frequency of fixation of neutral mutations in time depends only on the mutation rate, of which it is assumed that it is roughly constant during phylogenesis for most organisms, it is possible for biologists to determine the time that has expired from the moment of divergence of two sister groups (taxa) from the common exclusive ancestor on the basis of the number of substitutions that occurred independently in the two lines from the moment of divergence. If we sequence a certain DNA section for two related species and determine the number of neutral mutations in which they differ, on the basis of a mathematical model that takes into account and eliminates the effect of possible repeated mutations in the same position, we can estimate how many fixation events occurred in the two species from the moment when they branched off from the common ancestor. If, in addition, we know the characteristic substitution rate for the given taxon and the given gene, i.e. the average number of mutations fixed for the given species per time interval, then we can calculate the time that has elapsed since the branching off of the relevant phylogenetic lines. Thus, fixation of neutral mutations can act as a molecular clock, permitting more or less exact dating of the individual events in phylogenesis or, to be more exact, the individual splitting events that occurred during the cladogenesis of the studied taxon.

            It is obvious that this substitution rate is frequently not known. However, in this case, we can calibrate the molecular clock on the basis of the number of evolutionary changes in which the two studied species differ from a third species for which we know the moment of divergence from the paleontological record (Fig. IX.6). If, for example, we know that the taxon including species A and B branched off from the taxon including species C at time T₁ ago and, since that time, species A has collected K_AC mutations in the studied gene and species B K_BC mutations, where, since the time of splitting off of species A and B, i.e. over time T₂, species A and B collected K_AB mutations, we can calculate the time expired since divergence of species A and B according to the equation

T₂ = (2K_ABT₁) / (K_AC + K_BC)

If, on the other hand, we know the time that has expired since branching off of species A and B and we are interested in the time that has expired since the splitting off of these species from species C, we can use the equation

T₁ =( K_AC + K_BC) T₂ / 2K_AB

Contemporary data and the current theory indicate that the rate of molecular evolution can increase substantially at the moment of speciation. Extensive studies performed on the representatives of a series of taxa have shown that the number of speciations can explain about 22% of the nucleotide substitutions in the DNA of two sister lines. In other words, the nucleotide divergence of two species does not depend only on the time that has elapsed since splitting of the two lines from the last common ancestor, but also on the number of speciations that the ancestors of the two species have undergone since that time (Pagel et al. 2006).  It is quite possible that acceleration of anagenesis in populations that underwent peripatric speciations (Flegr 2008) leads to fixation of many positive mutations by selection and a great many neutral and weakly detrimental mutations through the mechanism of genetic draft.

see Host specificity

Most of the definitions of species require that the individual species be monophyletic, i.e. that they be formed in evolution through a unique speciation event. The definition of a typological species, at least in principle, does not entail this limiting requirement. A taxonomist usually considers that a separate species corresponds to a line of organisms that differ from other similar lines in an important phenotype trait. However, what an important phenotype trait consists in is often a matter of the subjective opinion of the scientist. Frequently, a quite inconspicuous trait is chosen, whose presence or absence has some sort of importance for humans. Amongst bacteria, this trait frequently consists in the ability to cause a certain disease or cause a certain symptom of a disease. As the genetic basis for such a trait in the individual lines of organisms need not be very complicated, its occurrence need not be correlated with the overall relatedness of these lines. For example, intestinal bacteria of the closely related species Escherichia coli, which exhibits pathogenic activity for humans, is frequently included under the bacterial genus Shigella. The genus was defined primarily on the basis of its pathogenicity; however, immobility and the inability to cause fermentation of glucose are used as diagnostic traits. In time, it was found that these traits need not always be correlated with the pathogenicity of these bacteria. Consequently, a great many pathogenic strains of Escherichia coli are now known. Molecular taxonomy studies later demonstrated that the genus Shigella is apparently polyphyletic and that its individual lines are variously scattered throughout the phylogenetic (more precisely genealogical) tree of the species E. coli (Pupo, Lan, & Reeves 2000) (Fig. XX.6).
While most modern definitions of species recognize only a monophyly as a species, i.e. a related line of the population derived from a single original parental population, it is almost certain that some biological species are formed polyphyletically, i.e. their members evolve several times independently within various populations. A typical example consists in botanical species formed by polyploidization of some existing diploid species (see XXI.5.2). Polyploid plants exhibit a different phenotype from their diploid ancestors and can also generally not cross with the original species because of differences in the number of chromosomes (however, some species of plants are capable of this across several ploidy levels (Petit, Bretagnolle, & Felber 1999)). However, they are usually capable of productively crossing with independently formed plants with the same ploidity level, i.e. with plants that have the same number of chromosomes. Tetraploids formed by duplication of the genome of a diploidal inter-species cross have relatively the greatest chance of full renewal of fertility. Their chromosomes will most probably not form an aberrant chromosomal arrangement containing tetrades during meiosis, but rather regular chromosomal arrangements containing twice the number of chromosomal pairs compared to the original diploidal species. It is apparent that some polyploids can be formed repeatedly within a species, and can successful reproduce together because of having the same number of chromosomes. As a consequence, they comply with the requirements of the definition of a biological species although, for example, they do not comply with the requirements of the definition of a phylogenetic species.

Reproductive isolation barriers internal

see Stopping the Muller's ratchet hypothesis of advantage of sexuality 

Mutations are random changes in the sequence of nucleotides that occur mainly during replication or during repair of damaged nucleic acids, in most organisms in the double-helix DNA molecule. These mutations are random in direction and in the degree of their affect on the phenotype of the organism, however not in the sites of their occurrence or in their molecular nature, i.e. whether nucleotide substitution (insertion, deletion) or inversion of part of the DNA strand occurs. As we showed in Chapter III (Mutations), the type of mutation and the probability of its occurrence at a certain position in the nucleotide strand depend not only on the nucleotide that is present in the given position, but also on the nucleotides or sequence motifs that occur around this position. However, the types and frequency of mutations are also related to the mechanism of replication of the given DNA segment. Other mutations are formed in a continuously replicated strand (leading strand) and others in a discontinuously, through Okazaki fragments, replicated strand (lagging strand) (Lobry 1996). Mutation processes are also affected by whether the given segment is, or is not, transcribed and thus whether it is present in the cell temporarily in the single-strand or more or less permanently in the double-strand form, whether it is wound around the nucleosomes or whether it is located at a site between two neighbouring nucleosomes (Francino & Ochman 1997; Tillier & Collins 2000; Szczepanik et al. 2001; Holmquist 1994). 

The process of preferential formation of certain types of mutations in certain positions in the nucleotide strand is most frequently called mutation bias. In some works, this process is also called mutation pressure; nonetheless, this term should not be used in this sense, as it has long been used by geneticists and evolutionary biologists for another phenomenon that, however, occurs at the level of populations – the repeated formation of the same mutation in the population. As a large fraction of mutations occur during reparation processes, reparation drive is mostly recognized as an independent process.

It is highly probable that mutation bias and reparation drive and not, e.g., natural selection, genetic drift or genetic draft are responsible to a major degree for evolution of the overall structure of the genome, i.e. for its increase or decrease in size, changes in the content of GC pairs, formation of isochore structures and similar phenomena (Holmquist & Filipski 1994).

At the present time, mutation processes are considered to be a natural and essential part of Darwinistic evolution. However, at the beginning of the 20th century, this point of view was far from being a matter of fact and there was even a separate evolutionary theory, termed mutationism, which was considered by its proponents to be an alternative evolutionary theory that was incompatible with Darwinism. For example, when an orthodox mutationist explained the formation of wings in the ancestor of a certain clade of winged insect, he based his arguments on the concept that the members of the relevant clade of the wingless species produced winged mutants more rapidly than these mutants produced wingless individuals – revertants. Thus, winged individuals occurred in nature with increasing frequency until they completely predominated in the given clade.
Mutationists diminished the importance of natural selection and were willing to consider it to be, a most, a factor that removes unsuitable mutations. They overlooked the fact that, in the absence of this factor, they are not capable of explaining the most interesting phenomenon in biological evolution, i.e. the formation of adaptive traits, complicated yet useful structures and patterns of behaviour.

Other categories of mutations, genome mutations, affect entire chromosomes or entire chromosome sets. In contrast to the previous types of mutations, these mutations are not formed as a consequence of irregularity in DNA replication or repairing, but as a consequence of irregularities and errors  in the progress of cellular division. As a consequence of these disorders, organisms can be formed in which a certain chromosome is multiplied or, on the other hand, is lacking (aneuploidy); in other cases, the entire chromosome series is multiplied (polyploidy). Depending on the number of specimens of a given chromosome occurring in the cell, this can correspond to nulisomics, disomics, trisomics, etc. On the basis of the number of chromosome sets, these are then haploid, triploid, tetraploid, etc. organisms. It was found in a study of human sperm that the frequency of diploid sperm varies around 0.2% and the frequency of haploid sperm with multiplication of one of the four monitored chromosomes varied from 0.1 to 0.17% (Miharu, Best, & Young 1994).

In most animals, the sex of the organism is determined by the gene dose and individuals with aberrant autosome ratios and sex chromosomes have transitory traits between males and females, i.e. are intersexes, and are mostly not capable of reproduction. Analogous disorders can occur for uneven gene doses at various chromosomes (cf. the Down syndrome in human beings, caused by trisomy of chromosome 21). Thus, these mutations are of only limited evolutionary importance for animals. However, the situation is very different, for example, for plants, in which the gene dose does not play a role in determining the sex and in which polyploidy thus generally does not have a detrimental effect on the viability or fertility of the mutant (Muller 1925).

A large proportion of these extensive genome restructurings cause partial or complete sterility in their bearers or at least form very effective interspecies barriers.However, polyploidization is simultaneously a mechanism that enables hybrid speciation.If two species cross, the zygotes cannot normally develop, because the gametes of the two species contain different sets of chromosomes.Thus, during cell division, they cannot form regular pairs of homologous chromosomes, so that the two chromosome sets divide unevenly into the daughter cells.As a consequence, most cells are not viable.However, if polyploidization occurs prior to hybridization, either autopolyploidization as a consequence of mitosis, which is not followed by cellular division, or alopolyploidization as a  consequence of fusion, e.g. of two diploid cells derived from two different  species in a single tetraploid cell or, more frequently, through a triploid intermediate stage (see XXI.5.3), the situation is substantially more favourable.If, for example, two tetraploid organisms cross together, their gametes already contain pairs of homologous chromosomes, so that a quite regular dividing spindles are formed during cell division and the chromosomes can be divided completely evenly amongst the daughter cells.Examples of hybrid speciation are encountered very frequently in some families of plants and also in animals with parthenogenetic reproduction, for example in some daphnia (Daphnia) (Dufresne & Hebert 1994).

Mutations at the level of the entire chromosomes – Translocationsof major extent can even be manifested in the structure of entire chromosomes.Simultaneously, classical cytogenetic methods can be employed to determine the occurrence of fusion or fission of chromosomes, i.e. processes entailing a change in the number of chromosomes in a chromosome set without a simultaneous change in the amount of DNA in the genome.A change in the number of chromosomes is not usually manifested in the phenotype of the organism, but often acts as a strong interspecies barrier.

Robertson transloctionis an interesting type of chromosome mutation in which one chromosome with a centromere in the vicinity of the centre (metacentric chromosome) is formed from two chromosomes with centromeres in the vicinity of the ends of the arms (metacentric chromosomes) (Fig. III.4).However, the altered karyotype contains one less chromosome, where the number of chromosomal arms does not change.There are a number of species, the best known of which are, e.g., the house mouse, in which the occurrence of local populations with one or more Robertson translocations is very common (Zima et al. 1990).It is very probable that meiotic drive is responsible for spreading of these chromosomal mutations (see VI.3.5) (Zimmering, Sandler, & Nicoletti 1970; Prout, Bundgaard, & Bryant 1973; Thomson & Feldman 1974), i.e. a phenomenon in which meiosis does not occur completely evenly and one of the pair of homologous chromosomes enters the sex cells preferentially.In case of polymorph populations, in which a certain chromosome with a Robertson translocation occurs and simultaneously two original unfused chromosomes are present in other individuals, it can readily happen that, in a heterozygote with two acrocentric and one metacentric chromosome, the metacentric chromosome will enter the sex cells with greater (in other species with lower) probability during meiosis (Gropp, Winking, & Redi 1982; Everett, Searle, & Wallace 1996).In this case, the particular type of chromosomes will spread in the population even under conditions when the heterozygotes will have reduced fertility compared to the original parent form because of the formation of part of the gametes with an incomplete (aneuploidal) chromosomal set – cf. the blue beard model (IV.9.1).