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Variability

Variability is the ability to produce variants.In order for a system to be able of becoming a subject of natural selection, it must contain elements that are capable of changing over time, of producing variants differing in smaller or larger details. Variability can again be realized in various ways. In modern organisms, mutations occur as the main source of variability, i.e. errors usually occurring during the replication or repair of DNA.

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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

Vectors and virulence

see Horisontally transmitted parasites and evolution of virulence

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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

Vertical transmission of parasites and virulence

By definition, a parasite reduces the fitness of its host. Consequently, genealogical host lines infected by a vertically transmitted parasite are at a disadvantage compared to uninfected lines. As a result, these lines and their parasites should sooner or later disappear from the population. If a vertically transmitted parasite is to survive for a long time in the population, it must have specific mechanisms formed for this purpose.
            One of the ways in which a vertically transmitted parasite can ensure survival in the population is by placing those individuals in the host population that are not infected at a disadvantage. Yeast killer factor, dsRNA-viruses transmitted primarily vertically in the population, from parents to offspring, are typical representatives of parasites employing this strategy. The double-helix RNA of these viruses encodes both a toxin excreted by the infected cell into its surroundings and killing yeasts of the same or related species, and also an antitoxin that protects the infected host cell against the action of the toxin. The infected yeast cells expend a major part of their resources for synthesis of the RNA of the killer factor and molecules encoded by this RNA and thus multiply more slowly than their uninfected competitors. Simultaneously, however, in contrast to the unattacked yeasts, they are not killed by the toxin, which, of course, places them at an advantage in intraspecific competition.
            Another possibility that is sometimes utilized by parasites is to become indispensible for the host organism. In this case, the parasite does not harm the competitors of the infected host, but “punishes” a host that manages in some way to get rid of the parasite. A number of parasites employ this “drug-dealer strategy”. The restriction-modified systems (RM-elements) of bacteria are a typical example (Fig. XIX.9). (Jeltsch & Pingoud 1996). In this case, the relevant genetic element (transposone-type genome parasite) both encodes the methylase enzyme methylating a certain short oligonucleotide, for example hexanucleotide, wherever it occurs in the bacterial DNA, and simultaneously also encodes the restriction endonuclease enzyme, which splits the same oligonucleotide if it is not methylated. When the RM-element enters the bacterial cell, it first synthesizes methylase molecules according to it and they then methylate all the relevant sites occurring in the bacterial DNA. After some time, the restriction endonuclease molecules also begin to be synthesized. As, at that time, the endonuclease target sites are already methylated, the bacteria are not harmed by their presence. However, if the bacteria were to get rid of the RM-element some time in the future, both the methylase and the endonuclease molecules would cease to be synthesized. Division of the bacterial cell would gradually lead to a reduction in the concentrations of both enzymes and, as soon as the methylase concentration were reduced sufficiently that at least some of the enzyme target sites would remain unmethylated, the endonuclease would cut the bacterial DNA at these sites and kill the particular cell. This mechanism ensures that rapidly multiplying bacteria that lose this element would not be able to predominate in the population of the particular bacteria in the future. RM-elements were originally considered to be a sort of immune system of the bacteria directed primarily against viruses. However, they do not seem to be particularly advantageous for this function. It is not functional against RNA-phages or against phages with a single-strand DNA-genome, many endonucleases cannot find the relevant sensitive sites in the short phage genomes and, in addition, there is a substantial probability in large bacteria populations that at least some of the phages would acquire the relevant methylation protection prior to splitting and would thus eliminate the relevant defense system of the bacteria in their offspring. Study of some sequences of bacteria and phages has actually shown that palindromes (potential target sites of RM-elements) are eliminated in the genome of bacteria more than in the genome of their phages (Rocha, Danchin, & Viari 2001; Kobayashi 2001).
A great many parasitic bacteria apparently employ a similar strategy, although not in such a drastic form. The existence of the drug-dealer strategy to a certain degree obscures the difference between parasites and mutualists. While symbionts help their host to survive, it somehow caused this dependence of the host on their assistance in the past. For example, it has been observed that, after Amoeba proteus strain D amoebas were infected with rod-shaped bacteria in 1966, their rate of multiplication decreased substantially. However, after several years, the presence of the bacterial endosymbionts ceased to harm the hosts and the amoebas even became dependent on it. When the amoebas were treated with a suitable antibiotic that killed the bacteria, they lost their ability to reproduce (Lee & Corliss 1985). A similar situation apparently also occurred for some helminthes, e.g. filarial, that were infected in the past by bacteria of the Wolbachia genus. It is known that filariasis can be treated with tetracycline, at least in laboratory experiments, where its effect consists in elimination of bacterial symbionts from helminth cells (Dedeine et al. 2001; Stevens, Giordano, & Fialho 2002).

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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

Viral theory of background extinction

see Extinction, viral theory of background extinction

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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

Virulence

The rate of reproduction of the parasite in the host organism and especially the rate of production of the infectious stage of the parasite are extremely important parameters capable of affecting the efficiency of transmission of the parasite from one host to another. As the multiplication of the parasite has a negative effect on the viability of the host, the rate of multiplication is a subject of optimization rather than maximization. In this connection, it is usually stated in the biological literature that a well-adapted parasite does not damage its host much and thus there is a gradual reduction in the pathogenicity and virulence of the parasite during the coexistence of the parasitic and host species. However, the situation is somewhat more complicated. Adaptation of the parasite to the host population is related primarily to maximization of its infectiousness. Infectiousness, i.e. the ability to infect further individuals of the host species, pathogenicity, i.e. the ability to damage the health (vitality) of the infected host, and virulence, i.e. the ability to reduce the fitness of the host, are generally related in some way; however, this connection need not always be a close one (Combes 2001). Infectiousness need not always be correlated with the rate at which the parasite reproduces in the host and the kind of infectious stage it produces. In some cases, a smaller number of progeny with sufficient resources can infect a greater number of new hosts than a greater number of progeny that are less well equipped for life. The rate of reproduction is very frequently positively correlated with the pathogenic manifestations of parasitosis. Pathogenic manifestations of parasitosis mostly shorten the time of survival of the host. Consequently, a rapidly reproducing parasite is frequently capable of producing a smaller number of progeny during the lifetime of the attacked host than a parasite that reproduces more slowly.
 Simultaneously, the pathogenic manifestations of parasitosis almost always reduce the fitness of the host. However, the correlation between pathogenicity and virulence can sometimes be very loose. For example, a number of parasites mechanically or hormonally castrate their hosts. These castrators reduce the fitness of their hosts to zero, without in any way reducing their viability. Cases have been described where redirecting the resources of the host from the sex organs to its somatic tissues even increased the viability of the host (see XIX.6.3).
In some cases, host individuals that are more sensitive to the pathogenic action of the parasite have greater inclusive fitness than more resistant individuals. The fact that they rapidly submit to infection means that they protect their relatives, bearing copies of the same genes in their genomes, against the parasite. At other times, pathogenicity allows the immune system of the host to successfully identify the parasite, so that individuals with clinical manifestations of parasitosis have, in fact, a better chance of recovering (and thus greater fitness) than infected individuals without clinical symptoms.
            It should be borne in mind that phytopathologists and physicians (probably with the exception of epidemiologists) employ the term virulence in different ways. Phytopathologists understand virulence to be the ability of a parasite to infect a certain strain of host, while physicians see this as the level of pathogenic manifestations of the infection. For the evolutionary biologist, the term virulence has two equally legitimate meanings – from the standpoint of evolution of the parasite, this describes the rate of reproduction of the parasite within the host and, from the viewpoint of evolution of the host, this corresponds to the degree of reduction of the fitness of the host by the particular strain (species) of parasite (Poulin 1998; Combes 2001).

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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

Volcanic theory of mass extinctions

Temporarily increased volcanic activity could also have caused some mass extinctions. A short period existed in the history of the Earth during the Phanerozoic when there were enormous outflow floods of lava over extensive areas. For example, approximately 250 million years ago in the area of Siberia, there was an outflow of 2-3 million km3 of lava during less than 1 million years. This turbulent geological event must necessarily have been accompanied by considerable changes in the chemical composition and physical state of the atmosphere and hydrosphere, with a substantial impact on the global weather and subsequently also on the global biosphere (Officer et al. 1987).
Comparison of the time distribution of the greatest outflows of lava and mass extinctions indicated that a great many of them occurred at the same time (Renne et al. 1995; Kerr 1995; Kerr 2000). For example, the formation of lava traps in Siberia occurred at the same time as the period of the greatest known mass extinction at the end of the Permian and the lava traps in India were formed at the same time as the extinction at the end of the Cretaceous. However, in the latter case, it is now thought that this extinction was more probably caused by the impact of a cosmic body. However, it certainly cannot be excluded that the simultaneous occurrence of both catastrophes could have actually been the cause of the mass extinction and the hypothesis that there was a direct causal relationship between the impact of an enormous cosmic body and elevated volcanic activity should certainly not be rejected (Rampino 1987).
            Catastrophes of somewhat smaller extent but still sufficiently drastic could be related to explosive volcanism. Some authors (Rampino 2002) have suggested that super-eruptions occurred, on an average, every 50,000 years, with outflow of more than 1000 km3 of lava and more than 1015 tons of microscopic dust and aerosol particles. The destructive effect of such catastrophes, which was felt in changes in the climate even in the most distant parts of the Earth, would, in their extent, correspond to the collision of the Earth with a cosmic body with a diameter of 1 km; however, these catastrophes would occur roughly twice as often. From our selfish viewpoint of the possibility of survival of the human race, it is of fundamental importance that, in contrast to catastrophes caused by comets, where it may well be possible in the future to artificially avoid their pathways, there is apparently even theoretically no way of effectively defending ourselves against a catastrophe caused by the super-eruption of volcanoes.

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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

von Bauer’s first law of embryology

According to this law, in the ontogenesis of each species, the individual structures are formed gradually from structures that are common to all the members of the highest taxon to the structures of common members of gradually lower and lower taxa, to which the given species belongs. The historically older von Bauer’s law, which Darwin also mentioned as one of the important documents for the validity of his theory of evolution, is actually substantively more correct that the newer Haeckel’s recapitulation theory. However, there are many exceptions to both the recapitulation theory and von Bauer’s law. In a great many species, the route through which the ontogenesis of a certain structure reaches a certain stage can be modified and some stages can even be omitted in some species (see XII.7.3). It is, however, true that it rarely occurs that the order in which the individual stages appear is reversed and that there would thus be a flagrant breaking of von Bauer’s law and this also the recapitulation theory.

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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
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