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Ectoparasites

see Anagenesis in parasites

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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

Effect of the rare male

see Inertia of sexual selection

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Effective size of the population

In describing the dynamics of fixation of mutations, it is necessary to consider not only the probability with which a mutation will become fixed in a population of a certain size, but also the time required on an average for fixation of a mutation. The probability that a newly formed mutation will be fixed is equal to 1/2N. Similarly, the average time required for fixation of one mutation is proportional to the size of the population. However, this is a case of direct proportionality. M. Kimura derived that the average time for fixation of a mutation by genetic drift is equal to 4Ne generations, where Neis the effective size of the population (the effective size of the population is a term that will be explained in Section V.3.2.1) For a population with an effective size of 30,  fixation of a neutral mutation will thus require an average of 120 generation periods.

The graph describing the shape of the time distribution required for fixation of a mutation by genetic drift is highly asymmetric. The asymmetry of the graph reflects the fact that it is highly improbable that a mutation will become fixed sooner than in 0.8Ne generation periods and a great many mutations require substantially more time than the average 4Negeneration periods.

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Elbow room hypothesis of advantage of sexuality

The elbow room hypothesis assumes that polymorphism of offspring, which is renewed in every generation because of sexual reproduction, reduces competition amongst siblings. The fact that the offspring of common parents differ in a great many traits means that they have somewhat different ecological, for example food, requirements. Thus, they do not compete together as much as the identical progeny of an asexually reproducing organism.

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Eldredge

History of evolutionism – post-neo-Darwinist period

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Empedocles

see History of evolutionism - pre-Darwinist period

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Endocytobiosis

The closest form of cooperation and the closest interconnection  exists between intracellular endosymbionts, called endocytobionts, and their host organisms or, to be more exact, their cells. When the intracellular endosymbiont begins to be transferred from one host to another solely through the sex cells of the host, its fitness becomes completely dependent on the fitness of that host. This basically ends any further “arms race” between the host species and the endosymbiont, as the selection pressure on the creation of traits permitting an increase in its own fitness at the expense of the other organism completely disappears. From that moment on, it is advantageous for both species to only cooperate and the coevolution of the two species ends with the two species dividing up the individual biological functions so that the chimeric cell formed can work as effectively as possible (see XIX.5.5.1). This division of functions sometimes goes so far that both species eliminate, from their genomes, the genes whose function would  be doubled or even replace their own genes in the genome by the genes of their partner – symbiont. Important organelles of eucaryotic cells, including mitochondria and plastids, evolved through this mechanism, (Margulis 1981). However, extensive results indicate that the endosymbiotic formation of mitochondria and plastids was probably not the first symbiogenetic event in the history of eucaryotic cells. Comparison of phylogenetic trees formed on the basis of various proteins has shown that the actual nucleus of the eucaryotic cell was most probably formed as a chimera through the combination of genomes, probably from two symbionts, one of which was a related gram-negative eubacterium and the other an archaebacterium (Golding & Gupta 1995; Gupta 1998). Study of the metabolic pathways of contemporary organisms and their organelles leads to similar conclusions (Martin & Müler 1998)(Fig. XVIII.3). It could be speculated that it was an increase in the size of pre-eucaryotic cells (by a volume 3-4 orders of magnitude greater than the procaryotic cells) that became a pre-adaptation for the emergence, first of the ability to phagocytose larger particles of food and, in direct connection with this ability, also pre-adaptation for the emergence of endosymbiosis. A series of subsequent endosymbiotic events could finally have led to the formation of modern eucaryotic cells and subsequently of multicellular organisms (Flegr 1990). Such an increase in the size of a eukaryotic cell could be made possible, for example, by the formation of a mechanism that permits overcoming the limitation of the rate of biochemical reactions by the slow rate of diffusion of the individual reactants in the cytoplasm (Flegr 1990).

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Endoparasites

see Anagenesis in parasites

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Endosymbiosis

Endosymbionts and their hosts have gone very far in mutual integration. Endosymbionts live directly inside the bodies of their hosts. In the vast majority of cases, the symbiosis of the two organisms is so close that one species cannot survive without the other one and does not even occur in isolated form in nature – with the exception of the invasive stage of an endosymbiont and new-born young of the host, which have not had time to become “infected” by their parents or the environment. Ruminant ciliates and bacteria are known examples of endosymbionts, as are endiosymbiotic protozoa in the digestive tracts of termites.  In the absence of these organisms, the host organism would not be capable of utilizing its main source of food, plant polysaccharides, especially cellulose. However, symbionts in the digestive tract are also important for other species, such as humans. Experiments with rodents freed of microbial symbionts and kept permanently under these conditions have shown that these animals require, for their lives, approximately one third more food than animals kept under normal conditions (Hooper & Gordon 2001). The symbiosis of fungi and algae (or blue-green algae) in the form of lichens is an obvious textbook example. It is less widely known that, according to some (very bold) ideas, terrestrial plants are also actually a sort of inverse lichens, i.e. the products of ancient symbiosis between algae of the Charophyceae genus and a fungus. Here, the algae would provide the mechanical support, protection against UV radiation and a number of other functions and the fungus would provide the cytoskeletal apparatus required to prolong the growth of cells, employed, for example, in the growth of pollen tubes and hair roots (Atsatt 1993; Jorgensen 1993)
            Thus, very few species of animals can survive in the absence of endosymbiotic organisms. If nothing else, the symbionts at least provide them with some essential substances, for example some vitamins, that they are not capable of synthesizing themselves. However, in a great many cases, cooperation amongst the relevant species of organisms need not be especially close; the individual species of endosymbionts and the individual species of hosts can be mutually substituted.

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Environmentally directed mutations

Some species are capable of generating a greater number of mutations under certain, usually stress conditions. This allows them to overcome the unfavourable conditions. Some authors are of the opinion that the organism is capable not only of  generating a suitable number of mutations, but that it is also capable of generating just those mutations that allow it to overcome the currently active unfavourable environmental factor. In other words, according to these concepts, organisms are capable of environmentally directed mutations. The results of fluctuation tests, replica plating tests and our knowledge of the mechanisms of the formation of mutations indicate that, in general, organisms mutate randomly, and not in an environmentally directed manner.(see Fluctuation tests and Replica plating tests).  However, in a great many organisms, there exist specialized genetic mechanisms through which the organisms generate a certain, momentarily advantageous type of mutation in specific situations.These mechanisms permit the population of organisms to react adaptively in situations in which they find themselves repeatedly, although not very frequently.Contemporary evolutionary biology assumes that, similar to other adaptive processes or structures encountered in organisms, these mechanisms and necessary molecular apparatuses arise gradually through random mutations during evolution through the action of natural selection.

The hypervariability of the surface protein in the African trypanosome is an example of such a mechanism (Borst et al. 1997).During their life cycle in the organism of their host, these parasitic protozoa regularly and repeatedly encounter attacks by the immunity system.Most of these attacks are directed against the main antigen of the surface coat and the individual trypanosome is practically defenseless against them and is thus rapidly and reliably killed.  The defensive strategy of the protozoa lies in the fact that it has approximately 1000 genes for very different variants of this protein in its genome and, through mutations in the regulation regions of the individual genes, such as duplication translocation to the expression site, ensures that synthesis of the surface antigen is switched from one gene to the other in some individuals in the population.These events occur with relatively low frequency; at every instant in the body of the host, almost 100% of the protozoa express the same surface antigen.However, it is sufficient for at least several mutated cells with the minority antigen to survive the immunity response of the organism against the majority surface antigen.These again multiply in the host so that, sooner or later, it again develops a strong immune response against them.Less than 0.1% of the protozoa mostly survive the individual waves of immune response; however, the host is not able to completely rid itself of the parasite.A similar parasite strategy is also known for bacteria of the Borrelia and  Neisseria genera (Seifert & So 1988; Meyer 1987) and it can expected with certainty that it will be even more widely spread in nature.

Experiments have shown that antigen variability in parasites is actually ensured by hypermutability of specific DNA sections.The molecular mechanism of these mutations is quite well known and it is known that, for example in trypanosomes, they occur with a frequency of 0.01 and in borrelia with a frequency of 0.0001 – 0.001 per cell division.However, in some cases, the increased frequency of certain mutations can be only an apparent cause of a similar  phenomenon and the entire mechanism can function on the basis of some form of natural selection.An example could be the case of the formation of resistance against methotrexate through the multiplication (number of copies) of certain genes.If a gradually increasing amount of this inhibitor enzyme dihydrofolate reductase is added to long-term passage cultures of the protozoa Leishmaniamajor, or even to in vitro passage cultures of mammalian cells, in time a species of the protozoa (mammalian cells) is obtained that will be very resistant to this inhibitor.Study of the genome of these resistant species demonstrated that they have a multiple copies of the gene for dihydrofolate reductase (Schimke 1984; Grondin et al. 1998).A similar mechanism of formation of resistance is active for mosquitoes of the Culexgenus resistant to organophosphate insecticides (Callaghan et al. 1998).It is possible that this multiplication of genes occurs in the cell as a random mutation and is only anchored through natural selection under the condition of selection pressure from the inhibitor.However, it is also possible that a specific mechanism exists in the cells,which is capable of multiplying any genes whose transcription and subsequent translation to the protein molecule occurs at a velocity approaching the maximum velocity for the given gene.For example, if the enzyme dihydrofolate reductase is inhibited by the presence of methotrexate, the cell must synthesize a much greater number of molecules of the enzyme than a cell under normal conditions.Most of the molecules of the enzyme are immediately inhibited, so that transcription of mRNA from the relevant gene is regulated up to maximum possible rate.If the cell is capable of multiplying the gene for dihydrofolate reductase sufficiently so that it manages to compensate the inhibiting effect of methotrexate, transcription of mRNA will no longer have to occur at the maximum velocity and further multiplication of the gene will stop.

A very interesting situation can occur in the case of hypermutability of the variable part of the chains of immunoglobulins in B-lymphocytes (Berek 1992; Berek & Ziegner 1993).Here, the relevant processes occur at the intra-organism level and the relevant mutations are somatic mutations; however, all the processes are controlled by the same laws as similar processes at the inter-organism levels.

If the organism of a mammal encounters a foreign protein, at least some of its B-lymphocytes will bear, on their surfaces, immunoglobulin molecules with a certain, although frequently very low affinity for this protein.However, during a few days, the progeny of these lymphocytes begin to appear in the organism; they have individual mutations in the variable part of the genes for immunoglobulins that, as they regularly accumulate in the genes, gradually increase the affinity of the immunoglobulins for the given protein.It is said that the affinity of the antibodies matures through hypermutability of the genes for immunoglobulins.

It was originally assumed that, in this case, the immune system employs the classical mechanism of Darwinistic evolution, i.e. generation of quite random mutations in the relevant regions of the immunoglobulin genes and selecting mutants with immunoglobulins with greater affinity for a foreign protein.However, there are two unexpected facts.The generation time for lymphocytes is many hours, while the actual process of affinity maturation lasts only a few days.Simultaneously, the number of selective intermediate stages and the number of mutations that must be gradually fixed is so large that it is practically impossible for the whole process to take place during a few cell generations, during which the process of antibody affinity maturation occurs (Manser 1990).In addition, when the individual mutants were studied as they were formed during affinity maturation, it began to be apparent that every mutation that was fixed increased the affinity of the immunoglobulins compared to the former state (Lavoie, Drohan, & Smithgill 1992).If the Darwinistic mechanism were active, we would expect that a substantial percentage of the mutations would be neutral, at the very least.

At the present time, there is only one model that has attempted to explain this paradox in the behaviour of the immune system during antibody affinity maturation (Manser 1990).The affinity matures in the germinal centres of the lymphatic nodes (Fig. III.9).At these sites are located populations of B-lymphocytes and auxiliary T-lymphocytes and also a certain amount of the antigen, for example a foreign protein bound to the surface of the dendritic cells in the follicles.The B-lymphocytes bind the antigen released gradually from the dendritic cells to their surface immunoglobulins and transport it to their lysosomes.There, they split it enzymatically into the individual peptides, bind these to II class MHC (major histocompatibility complex) molecules and, together with them, transport it back to their surface.The T-lymphocytes “feel out” the surface of the B-lymphocytes and provide a growth factor to those that present the greatest number of foreign peptides on their surface.Only B-lymphocytes that have obtained the growth factor can divide.If all the B-lymphocytes have molecules of the same immunoglobulin on their surface, then they bind them all, internalize them, split them and present the foreign antigens on their surface to approximately the same degree.The assistance that is provided by the T-lymphocytes is thus also evenly divided and all the cells can divide only very slowly or do not divide at all.In contrast, if there is amongst the cells a mutant that produces immunoglobulins with greater affinity for the antigen, they preferentially capture this antigen from the other B-lymphocytes, present more foreign peptides on their surface and thus obtain more growth factor from the T-lymphocytes at the expense of the other B-lymphocytes and can thus divide more rapidly.

So far, this was an example of classical Darwinistic evolution of which we have, however, already stated that it cannot adequately explain the process of affinity maturation because of the inadequate number of generations of lymphocytes and absence of neutral mutations.The authors of the alternative model (Fig. III.10) assume that the cells must mutate in the quiescent state, i.e. when they are not dividing and, in addition, those mutations that do not lead to increased antigen affinity must be repaired.One of the mechanisms through which the lymphocytes could achieve these goals is as follows:The lymphocyte is capable of somehow generating mutations solely in the (+)-chains of the DNA of the gene for immunoglobulin, i.e. in the chain from which the mRNA for immunoglobulin is transcribed.After some time, both DNA chains are fitted together and the sequence of nucleotides in the (+)-chain is repaired according to the sequence in the (-)-chain.However, if one of the mutations is manifested in an increase in the affinity of the immunoglobulin for the antigen, then the B-lymphocyte obtaines the growth factor from the auxiliary T-lymphocyte and divides before the mutation in the (+)-chain can be repaired.As soon as replication occurs in the given DNA section, the mutation is definitively fixed in one of the two daughter cells and cannot be repaired.

This hypothetic model is only one of a number of possible models (Steele, Rothenfluh, & Blanden 1997).It will be interesting in the future to learn which mechanism was actually chosen by evolution to enable the immune system to avoid the greatest drawbacks of Darwinistic evolution, the inability to generate targeted (environmentally directed) mutations.

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Epigenetic information

Genetic information is defined as information entered in the primary structure of a nucleic acid, i.e. in the order of the nucleotides in the DNA molecule or (in some viruses) in the RNA. However, organisms also contain a large amount of further information in the structures of their cells and multi-cellular bodies, which also co-determine the course of all the molecular, biochemical and physiological processes, including ontogenesis, and thus co-determine both the characteristics and the behaviour of the organisms. This is called epigenetic information.

The entire molecular apparatus of the cell determines which DNA sections will be transcribed to the RNA at a given moment and which RNA molecules will be further translated to proteins.  If an important regulation molecule were missing in the zygote, the course and result of the ontogenesis of the given organism could be seriously disturbed and altered, even if the genetic information in the zygote gene pool is not disturbed. According to some authors, the importance of the molecular apparatus interpreting the genetic information for the progress of ontogenesis is similarly important as the genetic information located in the genome.

It cannot be denied that, for setting into motion and directing the individual development of an individual, the presence and functioning of both components is absolutely essential. Interventions into any of them can lead to similarly important influencing of the progress and results of ontogenesis. Nonetheless, from an evolutionary standpoint, genetic information encoded in the primary structure of the nucleic acid plays a quite primary and incomparably important role. A random change in the molecular apparatus of a cell can, of course, affect the result of the relevant ontogenetic processes, i.e. the characteristics of the particular individual. However, it is very probable that the changes caused in the characteristics of the organism would lead to repetition of the same changes in the molecular apparatus of the cells in the offspring and that the given change would be transferred to further generations. In certain, quite exceptional cases, the particular change can cause the occurrence of the same changes and thus be passed on from one generation to the next. An example could consist in prions, protein molecules that can adopt two different conformations, where the presence of the less common of them can induce the transition of other molecules to this conformation. However, only a negligible percentage of molecules or other cellular structures have this characteristic and thus it cannot be expected that heredity based on this principle could occur to a greater degree in evolution. In contrast, if mutation occurs in the DNA, the relevant change is automatically transferred, because of universal copying of the primary DNA structure during the replication, to subsequent generations, and causes the same changes in ontogenesis in progeny organisms as it caused in the parent organisms. While primary those genetic changes that are in some way advantageous for their carriers have a chance to be fixed evolutionarily, only epigenetic changes that are not only advantageous, but also cause their own occurrence and can thus be transferred from one generation to the next, have a chance of evolutionary fixation. Put simply, all DNA changes have high heritability, but epigenetic changes in the molecular apparatus interpreting genetic information have much lower heritability, generally approaching zero, in the vast majority of cases. As the heritability of changes is an essential condition for the functioning of biological evolution, especially the formation of adaptive characteristics of organisms, it is almost certain that genetic and not epigenetic information acts as the main medium for the evolutionary memory of contemporary organisms.

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Epigenetic inheritance

Epigenetic changes also include modification of the DNA and proteins bound to it through methylation, acylation or bonding through other reaction groups based on nucleic acids or on the aminoacids of chromosome proteins. Some of these changes are also transferred to further cellular generations. For example, cells may contain specialized enzymes that search for places in the DNA where one of the chains is methylated. They then methylate the second chain from these hemimethylated sites. If replication occurs in a certain DNA section, then these enzymes methylate the newly synthesized chain and thus renew the relevant methylation signal. Methylation of the regulation areas of some DNA sections can negatively or positively affect their transcription and the relevant regulation changes are transferred to further generations in the given cellular line.

Functional and morphological differentiation of the individual cellular lines is of fundamental importance in formation of the bodies of multi-cellular organisms. The individual animal and plant tissues consist of specialized cells, where division of these cells or their more or less specialized precursors again yields the specialized cells of the relevant tissues. It is highly probable that most differentiation changes occur through covalent and noncovalent modifications of regulation areas of the individual components of chromatin. Obviously, other cellular structures can also become the carriers of epigenetic information. Especially the receptor apparatus of the external cell membrane decides to a substantial degree which signals the given cell can receive and to which it can react. Synthesis of receptors, which enable receiving of the given signal, can also be part of the response to a particular signal. This means that the relevant differentiated state of the cells of a certain line is spontaneously maintained over time without requiring any modification of the actual cellular DNA. According to some authors, the formation of specialized mechanisms of epigenetic inheritance permitted the formation of complicated multicellular organisms.

In a number of organisms, mechanisms of epigenetic inheritance are also involved in the transfer of phenotype plasticity traits from one generation to the next. The greatest numbers of examples of epigenetically inherited phenotype modifications are known for plants. For example, the morphology of individual flax plants differs very substantially according to the amount of nutrients in the soil, where the particular trait, gained during a single generation, is passed on through the seeds to the next generation. However, examples of similar phenotype modifications, which can be inherited even after a number of generations, are also encountered in some animals, especially those that reproduce asexually. Methylation and suppression of the cycloidea gene in the flax Linaria vulgaris, which demonstrably occurred at least 250 years ago and has been maintained by artificial selection to the present day, is probably the longest transferred (known) epigenetic modification. It is quite possible that many other known mutations actually correspond to epimutation – epigenetic changes inherited for a long time.

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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

Epigenetic processes

The development of a multicellular individual (ontogenesis) constitutes a set of extremely complicated and simultaneously precisely spatially and temporally coordinated steps.

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Epimutation

See Epigenetic inheritance.

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Epistatic interactions

Epistatic interactionsare interactions amongst genes occurring at different loci on the genome. The effect of a certain gene or some alleles of a certain gene is frequently quantitatively and qualitatively dependent on the presence of quite specific alleles in a completely different locus. Genes and thus also polymorphism in these genes can be functionally interconnected and the fitness of the bearers of certain alleles can be dependent, not on their frequency in the population, but rather on the frequency of certain alleles in completely different loci in the genome.

For example, if allele a1 of gene A is selectionally more advantageous (than allele a2) in combination with allele b1 of gene B and selectionally less advantageous (than allele a2) in combination with allele b2 and if polymorphism is maintained in gene B by any of the above-mentioned mechanisms (for example, selection for heterozygotes), then polymorphism will exist permanently in gene A (Fig. VIII.10).If, for example, a certain form of the enzyme were to function better in black two-spotted lady beetles and a different form in red lady beetles (for example, because, as a consequence of differences in the degree of reflection and absorption of solar radiation, the body temperature of dark-colored lady beetles in the sun were higher than that of red lady beetles), then both alleles of the relevant gene would remain in the gene pool of the species A. bipunctata for prolonged periods of time.

As most genes are apparently functionally interconnected in various ways, it can be assumed that epitstatic interactions will be very important in maintaining the polymorphism of a great many traits and, because of the existence of gene linkage, also the maintenance of polymorphism in selectively neutral traits (mutations) (Kel­ly & Wade 2000). See also Frozen plasticity theory.

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Ethological isolation mechanisms

see Reproductive isolation barriers internal

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Evolution

Evolution means the accumulation of changes in any system with a memory. A special for of evolution is the biological evolution, which is characteristic by involvement of natural selection.

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Evolution of a parasite

 

A parasite plays the role of an attacker in the evolutionary battle between a parasite and its host. This gives it a certain advantage – it can “choose the weapon”. Its second advantage is generally provided by its life strategy and its biodemographic (life history) parameters. Parasites leave provision of a major part of vegetative functions to their host organisms, so that they can invest a large portion of their resources into the production of progeny. Consequently, very many of them produce a great many progeny during their lifetimes (Combes 2001). For example, the hookworm (Necator) produces 15,000 eggs per day, some nematode worms (Ascaris) produce 200,000 and tapeworms produce (Taenia saginata) 720,000. This fact can have a fundamental impact on the progress and result of the evolutionary battle between the parasite and the host. If a species produces a great many progeny, of which only a small portion survive to reproductive age, then natural selection can act very effectively and evolution of adaptive traits can occur extremely rapidly. In addition, the fact that the generation period of a parasite is generally many time shorter than that of the host contributes to the fact that the evolution of a parasite occurs much faster than the evolution of its host.

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Evolution of behavior

 

Behavior can be defined in various, generally unsatisfactory ways. In this chapter, behavior will be considered to constitute the responses of different organisms to stimuli coming from their external and internal environment, where these responses most often consist in the changes of their position or in the position and state of their organs. The integration of signals and storage of the information that directs an individual’s behavior is not performed at the genome level, but at the level of specialized organs or organ systems and, in animals, especially at the level of the neural system. Behavior is basically an integral compound of the organism’s phenotype. In some cases, it is quite difficult to distinguish the point where the individual’s traits (morphological, physiological or molecular) end and its behavior begins. Even the body color, i.e. the part of its phenotype that, at first sight, definitely belongs to the category of morphological attributes, can be (and in animals often is) a result of the behavior of the organism – for example, the seasonal changes in skin color in beach volleyball players or similar, only slightly more spectacular changes in chameleons, cephalopods and some fish. Comparing the morphological attributes to computer hardware and behavior to software may seem to be a useful analogy. The genotype of an individual during the ontogenetic process determines the attributes of the organism. The way the organism will handle these attributes, how is it going to use the organs that nature has given it during the ontogenetic process, i.e. how is it going to behave, depends on its software. The same morphological structure (hardware) may be used for completely different purposes – the same beak can be used with the same success for shelling seeds or breaking snails out of their shells; prehensile primate limbs are even more universal. While the hardware, i.e. the body structure, remains practically unchanged during the adult’s lifetime (at least if we ignore the manifestations of wear and tear), the software can develop continuously; the individual is able to change its behavior, for example, as a result of accumulated experience. It is obvious that components of behavior exist that, in principle, resemble software, e.g., learned patterns of behavior whereas others are more reminiscent of hardware, e. g. inherited fixed behavioral patterns.

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Evolution of female preferences

The evolutionary mechanism of the emergence of secondary sexual traits – sexual selection – is relatively simple. This is true both for traits occurring on the basis of direct competition between the members of one sex (most frequently between males) and also for traits occurring on the basis of selection performed by the members of the opposite sex (most frequently females). However, an important question remains: what is the mechanism in females that fixes the tendency to prefer a certain type of male? This is especially true for those species where the striking sexual trait entails a reduction in the viability of the males and the actual process of selection of a male constitutes, at the very least, a loss of time for the females.
            At the present time, there are a number of theories that explain the emergence of female preferences. The oldest theory is based on Fisher’s model of co-evolution of male traits and female preferences; however, models of sensory drive, intraspecies recognition and models included in the group of hypotheses of good genes are also popular. It is very probable that all the considered mechanisms are valid to different degrees in various species.

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Evolution of mating types

The biological importance of the existence of functional anisogamy lies in the fact that it ensures that zygotes are not formed by combination of mutually related cells, in the extreme case gametes produced by a single individual (autogamy) but, where possible, by cells derived from different individuals (alogamy). However, the advantages of alogamy are not entirely apparent at first glance, especially the advantages for the individual. It can be advantageous for a population or the species as a whole if unrelated individuals can mate together. It holds more or less for most of the models that explain the existence of sexual reproduction as a mechanism increasing the evolutionary potential of the species that the favorable effect of sexual reproduction increases with increasing genetic difference of the mating individuals. However, for the individual, the inability to mate with the members of the same mating type is a limiting factor and thus generally disadvantageous. Thus, it is necessary to explain why individuals do not emerge in the population that would be capable of mating with all the members of their species, without respect to their mating type.

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Evolution of morphological anisogamy

If somatic cells fulfill the function of sex cells, as for unicellular organisms, then only functional differentiation of mating types usually remains. However, if the organisms form a specialized type of sex cell, gametes, for sexual reproduction, then functional anisogamy is generally followed by morphological anisogamy, differentiation of sex cells into microgametes and macrogametes. As their names indicate, microgametes are smaller and usually mobile, while macrogametes are usually many times larger and frequently immobile. In the typical case, the microgamete contributes only its genetic material to the formation of the zygote, while the macrogamete provides both its genetic material and cytoplasm. A number of hypotheses have been formulated to explain morphological differentiation of gametes into just two types (Matsuda & Abrams 1999).

            At least two contradictory requirements are placed on the morphology of gametes. On the one hand, the sex cell must contain a sufficient amount of cytoplasm and energy stores to ensure full functionality of the future zygotes; on the other hand, it should be as small as possible, either because a small cell is more mobile or because more small cells can be formed while expending the same amount of resources (Fig. XIV.1.). It is obvious that it is difficult to satisfy both these requirements simultaneously. As a consequence, a certain type of disruptive natural selection acts on gametes, leading sooner or later to differentiation of the cells into small “cheap” and mobile microgametes and large macrogametes (Parker, Baker, & Smith 1972).

            The fact that the microgamete generally does not contribute its cytoplasm to the future zygote constitutes a very important difference between macrogametes and microgametes. The fact that, during gametogenesis or during the fusion of the microgamete with the macrogamete, however at the latest following formation of the zygote, cellular organelles containing their own genome, i.e. plastids and mitochondria, derived from the paternal (however, in some taxons, from the maternal) line are usually eliminated (Birky 1995). Some evolutionary biologists are of the opinion that the necessity of eliminating extranuclear genetic elements is the main reason for formation of microgametes (Hurst & Hamilton 1992).

            It has been known for a very long time that extranuclear genes substantially affect the properties of a great many cells. It is, at the very least, striking that this effect very frequently does not bring the cells or organisms any adaptation advantage and is useful only for the carrier of a certain extranuclear genetic element at the expense of individuals that do not carry the given element. In a great many cases, the coding of the properties provides an advantage only for the actual element or for the organelle and is detrimental for its cell.

            Killer-factors in yeasts are a well-known, but not very typical, example because of their potential importance in interspecies competition. These are cytomplasmic genetic elements that encode a toxin killing yeast cells and simultaneously encodes the protein that provides the cell in which it is synthesized with resistance against the action of that toxin (Polonelli & Morace 1986; Boone et al. 1986). The killer-factor spreads rapidly in a population of yeasts. Yeasts that do not have it are rapidly killed when a yeast that contains this factor comes into their vicinity. The presence of the killer-factor is otherwise in no way useful to the yeast (outside of the area of intraspecies or interspecies competition). To the contrary, the necessity of synthesizing a large amount of extranuclear nucleic acid, envelope proteins (most  killer factor species have their nucleic acid protected by a special capsid) and finally also the toxin and resistance factor represent a substantial energy load for the cell. Factors causing male sterility in fruit flies and pollen sterility in some plants are similar examples that also spread in the population without bringing their hosts any advantage (Rieseberg 1994).

            The reason for this special behavior of extranuclear genetic elements is now clear. A competitive battle is constantly occurring in any genome between the various alleles of the individual genes. If these are nuclear genes, the individual alleles do not have much choice of strategy that they can elect in competition. With a few exceptions, most alleles can spread in the population only when they are capable of affecting the properties of their carriers so as to provide them with a selection advantage over the other members of the population. There are only a very few nuclear genes that have gained the ability in evolution to “cheat” the fair system of even distribution of genes derived from both parents during nuclear division (see Chap. VI). These genes are capable, for example, of causing gene conversion, overwriting a copy of the gene located on a homologue chromosome according to their own sequence. Another possibility is to destroy the homologue (to be more exact, homeological) chromosome derived from the other parent and cause that the organism be capable of producing viable germ cells with a certain chromosome derived only from one of the parents. The organism thus has reduced fertility, half of the gametes it produces are not viable, but the aggressive gene is contained in all the viable gametes and thus in all the progeny of the particular individual. For example t-alleles spread in the population of domestic mice in this way (Vanboven et al. 1996).s

            A different situation occurs if the gene is encoded on an extra-nuclear element, for example in the mitochondrial DNA. Under these conditions, during sexual reproduction through fusion of two full-value cells, any gene would be capable of spreading very rapidly in the population. Thus, it would be exposed to a strong selection pressure to “disobey the law”, in this case the law of “fair” distribution of the genetic material derived from the father and from the mother during meiosis and thus become an outlaw gene. For example, the gene can “learn” to somehow destroy its competitors, copies of the same gene on other genetic elements. Our contemporary knowledge indicates that extranuclear outlaw genes greatly complicate the functioning of unicellular sexually reproducing organisms. Various types of outlaw genes are formed in mitochondria and other genetic material containing elements that carry on a relentless struggle against one another, with detrimental consequences for the cells of this unicellular organism.

            The formation of microgametes is a very effective mechanism for stopping the spreading of outlaw genes located on extranuclear genetic elements. The fact that the microgamete transfers only nuclear material into the zygote, that it does not bring cytoplasmatic elements or subsequently destroys these elements, substantially reduces the possibility of the negative effect of outlaw genes derived from both parents within the zygote (Fig. XIV.2).

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Evolution of secondary sex ratio

Although a single male can frequently ensure the production of sufficient microgametes to cover the needs of the entire population, the ratio of the number of progeny of the male and female sex, i.e. the secondary sex ratio of the population, is close to one with surprising frequency. The mortality of males and females frequently differs during maturing and finally also in adulthood. Consequently, in adulthood, the tertiary sex ratio can be very different, usually biased in favor of females. In contrast, the primary sex ratio, i.e. the ratio of male and female zygotes immediately following fertilization of the eggs, is, to the contrary, usually biased in favor of the sex whose embryos die more frequently prior to birth. For example, in human beings, there are 160 male zygotes for every 100 female zygotes, while only 106 boys are born for every 100 girl babies (Dorak et al. 2002). It is obvious at first glance that a secondary sex ratio equal to one is not optimal from the standpoint of the population for a great many species. If more females were to be born at the expense of males and every male were to fertilize a greater number of females, the population as a whole could grow faster than when the numbers of males and females are approximately equal.

            This paradox has long drawn the attention of a number of biologists. Consequently, a number of hypotheses have emerged in to explain its existence. Hypotheses considering the same numbers of males and females to be a consequence of a genetic mechanism of determining the sex of the embryos are currently falling into disfavor. A genetic mechanism of determining sex should primarily affect the ratio of the two types of heterogametes and thus the ratio of male and female zygotes immediately after fertilization. This ratio, the primary sex ratio, however, frequently deviates substantially from a value of 1 and, as already mentioned above, approaches a value of 1.6 in favor of male zygotes in humans (Dorak et al. 2002). Similarly, comparative and experimental studies have demonstrated beyond the shadow of a doubt that a genetic mechanism of determining the sex of a zygote is extremely plastic at both the interspecies and intraspecies level. It is known that completely different mechanisms that, together, could theoretically ensure a quite arbitrary ratio of males and females in the progeny, exist in the individual taxa. Simultaneously, it is apparent that a population exposed to a selection pressure for a change in the sex ratio usually reacts quite easily to the given pressure and changes the sex ratio in the appropriate manner (Orzack & Gladstone 1994). It is thus apparent that a secondary sex ratio of 1 is not a consequence of the mechanism employed to determine the sex of the embryo but rather a result of quite specific selection pressures and that it is adaptive.

            A value of the secondary sex ratio equal to one can also be explained by the action of individual selection. The effect of this factor on the secondary sex ratio is expressed in the Shaw-Mohler principle (Shaw & Mohler 1953). Translated from the language of mathematics to normal language, this principle says that, at the instant when, because of the momentary ratio of males and females in the population, it is preferable to produce members of one sex rather than members of the other sex, those individuals, who produce more progeny of momentarily more valuable sex, will be at an advantage.

            Under normal circumstances, a population is in equilibrium in the numbers of males and females. The selection value of males (most readily expressed as the number of progeny that they leave behind) is the same as the selection value of females. Simultaneously, it is not important that all the females in the population have approximately the same number of progeny, while there are frequently enormous differences amongst males in the number of progeny. The variance value has no effect on the selection value of a member of a certain sex, only the value of the average number of progeny per member of that sex is important. If males predominate because of a random fluctuation in the population, then those individuals that, on the basis of their genetic predisposition, produce more progeny of the female sex are at an advantage. Thus, the population gradually returns to equilibrium. The temporary increase in the sex ratio amongst humans in the post-war years has been cited as an example of this phenomenon in the past. However, newer studies have shown that, for example, the men that returned to England from the battlefields of the Ist World War were more than 3 cm taller than those that died. As taller men exhibit a higher sex ratio in their progeny, the increased sex ratio in the post-war years can be fully explained by the higher death rate of shorter men in the military conflicts {13730}.

            It follows from game theory that the optimal strategy for an individual is to invest the same amount of energy into production of sons as into production of daughters. Under conditions where the production of sons is just as costly as the production of daughters, the ratio of young of both sexes in the population settles at a value of one.

            This explanation of maintenance of equal numbers of the two sexes was apparently first proposed by R.A. Fisher in 1933 (Fisher 1958). However, it must be admitted that later mathematical analyses of the relevant model demonstrated that establishment of equilibrium through such individual selection is too slow and that some other mechanisms are apparently also active in a great many species (James 1995).

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Evolution of Sexual heterochromosomes

Only unusually few genes have been identified on sex heterochromosomes, i.e. on chromosomes that occur only in cells of the heterogametic sex. For example, in humans, the gene determining hairiness of the ear lobes was, for a long time, the only gene whose position could be localized on the Y-chromosome using genetic methods. At the end of the last century, about 20 genes were known, of which 10 were expressed in the testicles and the others affected mainly secondary sex traits (Roldan & Gomendio 1999). Thus, compared to the other chromosomes, the Y-chromosome is very poor in genes.

            This state is apparently not accidental and a number of hypotheses attempt to explain it (Graves 2000). It is assumed that this could, for example, be a form of defense of the organism against a certain category of outlaw genes. The formerly described blue-beard model (see IV.9.1 and Fig. IV.10) is a hypothetical example of such a gene. The model assumes the existence of a gene on the Y-chromosome of a (heterogametic) male. The presence of this gene causes that the male kills all (or almost all) his daughters and feed his sons with their meat. Such a gene is, of course, disadvantageous for the population and the species and its presence will almost certainly be manifested in a reduction in the size of the population. However, in the subpopulation of males, this gene will spread almost without limits, as males with a Y-chromosome containing this gene leave behind more (and better-fed) sons than males with a normal Y-chromosomes. We do not yet know of a situation in nature that would correspond directly to the blue-beard model. However, we know a great many cases where an outlaw gene achieves the same effect of influencing the behavior, not of organisms, but of individual chromosomes during meiosis, i.e. the mechanism known as meiotic drive. The organism can then produce a far greater number of progeny of one sex at the expense of the number of progeny of the other sex, which can apparently even lead to extinction of the population in some cases (Carvalho & Vaz 1999).

            Genes on the X-chromosome are not exposed to such strong pressure to “favor” the members of the homogametic sex because their copies are also present in the genomes of members of the heterogametic sex. However, the cells of members of the homogametic sex contain two specimens of these chromosomes, while the cells of the members of the heterogametic sex contain only one. As a consequence, the genes on the X-chromosomes spent two thirds of the time from their evolutionary formation in the cells of homogametic individuals and only one third of their time in the cells of heterogametic individuals. Consequently, here too female analogues of the blue-beard model can be expected to a certain extent. For example, published studies have shown that grandmothers and aunts invest far more into the children of their daughters than into the children of sons {xxx, 12148}. However, it is not clear whether this is a result of the shared X-chromosomes or the substantially greater certainty in relation to the maternity of the children of daughters than the paternity of the children of sons.

            Evolution can, of course, not foresee the possible arise of outlaw genes and take the relevant counter measures in advance. Subsequent inactivation of any formed outlaw genes by inactivation of genes on mutually nonhomologous parts of the sex chromosomes is a far more probable mechanism of defense of organisms against outlaw genes. It will certainly be interesting to study the sequence of genes and pseudogenes derived from just these parts of the genome.

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Evolutionarily stable strategies

In a great many cases, the fitness of the bearers of a trait depends only very indirectly on its frequency. An increase in the frequency of a particular trait increases the fitness (and subsequently also the frequency) of the bearers of another trait, an increase in the frequency of the bearers of a different trait increases the fitness of the bearers of this other trait and this subsequently reduces the fitness of the bearers of the first trait. In these complicated interconnected systems, the fate of new mutations is decided not so much by the Darwinist fitness of its bearers as by whether the presence of the given trait is an evolutionarily stable strategy (ESS) in the sense of game theory. Evolutionarily stable strategy is considered to constitute strategy that, as soon as it predominates in the population, will be more successful in every situation than any other minority strategy (Maynard Smith & Price 1973). Thus, if an allele that codes behaviour of an organism (strategy) that is evolutionarily stable predominates in the population, then no other allele that occurs in the population through migration or mutation can force it out of the population – see the definition of ESS above.

A classical, albeit simplified example encompassing only two strategies in the basic variant, competition of only two strategies, on the basis of which evolutionarily stable strategy is studied, is the model of the dove and the hawk (Fig. IV.5).  Dove and hawk are names for two alternative strategies that can be adopted by two members of a single species when they clash, e.g., over a piece of food or some other scarce resource. The strategy of the dove consists in that the two individuals divide up the food. In contrast, the strategy of the hawk is dependent on the fact that the two individuals fight for the food, the winner gains the whole piece and the loser remains only with its injuries. If a dove encounters a hawk, it retreats without a fight (and thus without injuries) and the hawk gains all the food for itself. Changes in the frequencies of the two strategies are dependent on how successful its bearers are in competition with the other members of the population, i.e. how much food (and how many injuries) they gain from mutual encounters. If a hawk comes into a population of doves, it is initially very well off as it wins all the encounters without a fight and obtains all the food. The frequency of hawks thus increases in the population. Similarly, if a dove enters a population of hawks, it has an advantage in competition with the other members of the population. It always gives up in advance in any fight for food (however, it will certainly occasionally find some food when a hawk is not close-by); however, in conflicts with other hawks, an average hawk will end up with injuries in half the cases. It is apparent that, in the end, a stable ratio of doves and hawks will be established in the population, at which the average fitness of doves and hawks will be identical. The specific value of this ratio is determined by the by the values of the pay-off matrix. The following scheme gives an example of such a matrix. If two doves meet over a piece of food, each obtains an average gain of o/2 (where o is the average value of one piece of food expressed as input of biological fitness for the individual that consumes it). If two hawks meet, each of them gains, on an average, (o – c)/2 (where c is the average loss connected with injuries suffered in conflict of two hawks over prey, again expressed as the reduction in biological fitness of the injured individual). If a hawk encounters a dove, the hawk obtains gain o and the dove does not obtain any gain (but also suffers no loss). The average gain of a hawk in all conflicts (with doves and hawks) depends on the presence of the two strategies in the population and is equal to

 

(1)

 

where p is the frequency of hawks in the population. The similar average gain of a dove is

 

(2)

 

The population moves towards an equilibrium state, at which the average gain of the representatives of the two strategies is equal and where it holds that Zh = Zd. Substitution into equations (1) and (2) yields

 

(3)

 

Following simple modification, this equation yields the frequency of hawks in the equilibrium population

 

(4)

 

Neither the strategy of the dove nor the strategy of the hawk is evolutionarily stable. On the other hand, the strategy “behave like a hawk with frequency o/c and like a dove with frequency of (1 o/c)” is evolutionarily stable; if an allele that determines this behaviour predominates in the population, no other allele will be capable of successfully penetrating into the population. The basic model of the dove and hawk can be variously further developed (see also XVI.9). For example, interesting situations occur if we admit the existence of other strategies, such as the strategy “act like a hawk at the beginning of an encounter but, as soon as you encounter resistance, run away” or the strategy “act like a dove initially but, as soon as you are attacked, begin to fight like a hawk”. In some models, we find that a particular strategy acts as evolutionarily stable only until two different alternative strategies are present in the population; in other cases, the frequency of a certain strategy begins to increase but is completely forced out by some other strategy after a certain period of time (a strategy that had no chance of spreading under the initial conditions).

Most people erroneously understand strategy to refer to the particular behaviour of an animal or human being. However, the theory of evolutionarily stable strategies is certainly not related only to the evolution of individual patterns of behaviour. From the standpoint of the theory and the mathematical apparatus employed, it makes no difference whether we study the competition of the alleles that code a certain pattern of behaviour of their bearers, or alleles that code, e.g., the synthesis of a certain pigment or enzyme. Competition for an evolutionarily stable strategy is applied almost universally for sexually reproducing organisms. In these organisms, the fitness of the bearers of certain alleles is rarely determined by an unvarying selection coefficient, but is rather usually dependent on the frequency with which it encounters other alleles of the same or some other gene in the future embryos, i.e. on which alleles will probably be borne by both parents of the future progeny.

The fact that the advantageous or disadvantageousness of a certain strategy (in general a certain trait) depends on the frequency of alternative strategies (traits) in the population indicates that it is necessary to quite fundamentally reassess the original Neodarwinist concepts of the mechanisms of biological evolution.While the simple Neodarwinist model quite naturally assumes that the criterion of evolutionary success of a particular trait (characteristic or pattern of behaviour) consists in the average biological fitness of its bearers, contemporary theory indicates that, in the long-term perspective, the evolutionary stability of the given strategy is a more important criterion (given by patterns of behaviour or the presence of a particular trait).At the very least since 1973, when John Maynard Smith and George Price published the concept of evolutionarily stable strategy, this rendered completely irrelevant the popular dispute between the proponents and opponents of Darwinism as to whether the principle of natural selection and the principle of biological fitness are or are not circular definitions and whether Darwin’s explanation of the formation of adaptive traits is or is not a tautology from the standpoint of formal logic (see I.10.1)The development of the theory of evolutionarily stable strategy demonstrated that this explanation is primarily a scientific error – mutants whose mutated trait gives them greater fitness at the present time or in the future do not predominate in evolution, but rather mutants whose mutated traits represent evolutionarily stable strategy in the sense of game theory.We could, of course, begin to consider evolutionary stability to be a criterion of fitness.However, this would constitute a very fundamental redefinition of the Neodarwinist concept of fitness (as a technical term encompassing a set of quite specific and, under various circumstances, different characteristics affecting the chance of an organism to leave progeny, see I.10.1) and the term fitness would then really lose meaning to a substantial degree.

If we return to the original model of the dove and the hawk, we can see that, from the viewpoint of classical Neodarwinist theory, the dove strategy should win out in a structured metapopulation, as local subpopulations consisting of only doves would contain individuals with the greatest average biological fitness and migrants originating from this population would contribute to the greatest degree to the subpopulation of migrants, so that they would “infect”, with their genes, the greatest number of surrounding populations and would establish the greatest percentage of new populations.“Infection” of already existing populations would, however, be unsuccessful in a great many cases or would be only temporarily successful, as the dove strategy is not ESS.The theory of evolutionarily stable strategies shows that, in the long-term perspective, the substantially less advantageous mixed strategy from the standpoint of average biological fitness “behave as a hawk with probability p and like a dove with probability 1-p” is more successful.While this strategy is suboptimal from the standpoint of the average reward that the two individuals carry away from the encounter (compared to the average reward in a population consisting of only doves), it is, however, evolutionarily stable and, because the relevant population cannot be infected with any other strategy, it will, in time, predominate in all the local populations, and thus also in the subpopulation of migrants – potential founders of new subpopulations.

The concept of evolutionarily stable strategy thus apparently represents one of the deepest and most important blows to the very foundations of Darwin’s theory of evolution since the emergence of Neodarwinism.It is interesting and apparently quite significant that this aspect of the theory of evolutionarily stable strategies is currently not assigned its true worth and is even not much taken into account amongst evolutionary biologists.

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Evolutionarily stable strategy

An evolutionarily stable strategy is defined as a strategy that, once it prevails in a population, can never be overcome by another (minority) strategy (Maynard Smith & Price 1973). This is the strategy, that of all the alternative strategies, is most successful in competition with its own copies. Translated into the language of biologists, the long-term numerical prevalence of bearers of an evolutionarily stable strategy in the population is not threatened by the incidental appearance of mutants or migrants, because the bearers of any alternative strategy will have lower fitness than the bearers of the majority strategy. 
The best known model that can demonstrate the principle of competition of alternative strategies is the model called the dove and the hawk; it was described from mathematical point of view in another context in Sect. IV.5.1. The dove and the hawk are names for two alternative strategies asserted when two individuals compete over a certain resource, e.g. a piece of food.  If two individuals competing over a piece of food direct their behavior according to the dove strategy (for simplicity we will further talk only about two doves, two hawks, etc.), they will share the food and each gets, on an average, half of the reward. If two hawks compete, they will fight over the food and only one of them gets the whole piece; the other one will be injured more or less seriously with the negative value of the injuries usually prevailing over the positive value of the food acquired. The average reward that two hawks, the winner and the loser, get from their competition, is therefore negative. If a hawk meets a dove, the dove retreats without a fight, therefore without injury; the hawk gets all the food. An example of the pay-off matrix is given in Fig. IV.5. Analysis of the model shows that neither the dove nor the hawk represents evolutionarily stable strategies. If all the individuals in a population behave as doves, then the mutant, the hawk, wins all competitions without injury and the particular strategy will spread in population. Analogously, in a hawk population, the mutant, the dove, gets the biggest, i.e. zero reward from all competitions, because the hawks will mostly compete with other hawks so their average reward will be negative. It is obvious that finally a balance will be set up in the population entailing frequencies of both strategies where the dove’s average reward and the hawk’s average reward will be the same. If we admit the existence of mixed strategies, an evolutionarily stable strategy will be to behave with p1 probability as a hawk and with (1 – p1) probability as a dove.
Of course, the evolutionary stability of a strategy is only conditional; the given strategy is stable only under the conditions described in our idealized model. If, in a real population, a minority (mutated) new strategy occurred, one that was not included in the original reward matrix, the original winning strategy could easily lose its evolutionary stability. This limiting condition, obvious to a mathematician, is, of course, valid for any theoretical model; no model can predict the behavior of the system under conditions that were not considered while creating it.

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Evolutionary adoption hypothesis

Some authors assume that the relationship between a morphological trait that is useful from the viewpoint of specific behavior of an organism and the behavior itself is exactly the opposite of how it is described by the Baldwin effect. They assume that the relevant (incidental) phenotype change is primary and useful exploitation of the change by creating an appropriate behavioral pattern is secondary. Returning to the example in Chap. XVI.3.2, we find that birds with large strong beak first arise and that they then look for ways to use it and then, finally, by the trial-and-error method, they find that it can be used for shelling snails. According to these conceptions, in evolution,  the phenotype of organisms does not adapt itself to activities and the environment through adaptations, but rather by adoptions – by actively creating those behavioral patterns that best utilize the changes in the phenotype made by mutations and by seeking an environment where these phenotype changes can be best used (Piaget 1979; Ho & Saunders 1982).
            It may seem that both variants of the origin of usefulness are possible and even highly probable for adaptive traits that are conditioned by only one mutation. Actually, egression of the usefulness of adaptations by the Baldwin effect is much more probable. If a new mutation arises, e.g. one that leads to egression of a large strong beak, and the mutant would be lucky enough to find a way of using it sensibly, for example for cracking snails’ shells, it (the now useful mutation) can be passed on only to the organism’s offspring . However, it would be a prolonged and rather improbable process for the mutant’s offspring to prevail in population. Most – even very useful – mutations vanish from the population during a few generations because of genetic drift. If more mutations are required for the optimal value of the trait (the optimal beak size in our case), all of them have to appear in the offspring of the particular mutant. On the contrary, when the evolutionary novelty is made by the Baldwin effect, i.e. a particular behavior pattern is created first (birds start to crack the snails, even imperfectly because of a weak beak), this behavior pattern can spread horizontally into the whole population by imitation and the useful mutations (e.g. for a strong beak) can consequently arise in any individual. The speed and probability of development of evolutionary novelties by the Baldwin effect, i.e. by adapting the organisms to their environment and behavior through mutations, is much greater than if the organisms would have to look for an environment and behavior that would suit their mutations.

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Evolutionary biology

Evolutionary biology is branch of sciencethat studies the properties of the process of biological evolution and its individual specific mechanisms. Systematic biology andpaleontology study the actual history of the progress of evolutionary processes in a specific space and time, i.e. the course of phylogenesis.

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Evolutionary constraints

Evolutionary constraints are generally understood as properties of the structural elements of an organism that constrain the pathways that the evolution of the given species may or may not follow. Some biologists, called particularly by their opponents selectionists (functionalists, panselectionalists) are of the opinion that the only constraints that stand in the way of evolution follow from external constraints, i.e. from the laws of mathematics, physics and chemistry. If the existence of a certain structure is not excluded by the laws of the surrounding nonliving nature, then this structure (e.g. flying ears) must be formed in evolution through the effects of the relevant selection pressure. In other words, what is suitable and functional from an evolutionary standpoint and is not prohibited by natural laws will be formed sooner or later.

Other biologists, frequently designated as structuralists, on the other hand, think that certain mutations and thus certain structures can never be formed as, objectively, there exist certain internal constraints, barriers that evolution cannot overcome. In the extreme case, they state that the direction of macroevolutionary development is determined by just these evolutionary constraints, which decide which genetic changes will occur in the particular species. In macroevolution, they attribute a secondary and passive role to selection; according to them, it cannot form new evolutionary forms, but can only constrain the fixation of new forms that are unsuitable from the standpoint of survival of the organism or can hinder this.

According to structuralists, an important category of evolutionary constraints consists in the (evolutionarily) historical internal constraints, specifically ontogenetic constraints.These constraints determine which structures can or cannot be formed in the context of the existing ontogenesis. For example, if a certain pattern on butterfly wings is formed by the diffusion of a morphogen from a single place and if, after a certain time, individual dyes begin to be formed at places with certain concentrations, it is clear that only concentric patterns can be formed on the wings and not patterns of a different type (Beldade & Brakefield 2002). It is apparent that, if a certain structure cannot be formed in ontogenesis, it can also not become fixed during the course of evolution.

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Evolutionary constraints

- The effect of evolutionary constraints is another mechanism that can cause an evolutionary trend. Evolutionary constraints can, to a substantial degree, determine the character of the variability that will appear in a certain species and thus also the character and potential direction of anagenetic changes that can occur in a particular phylogenetic line as a result of the action of natural or species selection. As the relevant ontogenetic mechanisms of the daughter species are inherited from the parent species, the relevant evolutionary constraints will also be inherited and the same trend will appear in all the species of a particular phylogenetic line. The existence or absence of evolutionary constraints is considered by some authors to be the main difference that permits mutual differentiation of two, at first glance similar, evolutionary phenomena, convergence and  parallelism. In both cases, the originally phenotype dissimilar species of organisms become more similar through the action of similar selection pressures. If the anagenesis of both species occurred with the participation of the same evolutionary constraints, the evolutionary trajectory of this change was similar. This phenomenon is termed parallelism. Parallelism is manifested in the existence of the same evolutionary trend in both lines. If evolutionary constraints were not active in the formation of a similar phenotype, because, for example, unrelated organisms with different ontogenetic mechanisms were involved, anagenesis occurred in each line through a different evolutionary pathway. This phenomenon is termed convergence.
Especially in the past, evolutionary constraints were considered to be the main driving force for most evolutionary trends. The actual phenomenon of the tendency of the members of a certain phylogenetic line to change during evolution in a certain manner independent of the selection pressures acting on it from without and thus manifested as an evolutionary trend, is called orthogenesis. Some proponents of the orthogenetic concept of evolution assumed that the source of the relevant internal tendencies of an organism is nonmaterial in nature, for example that this could consist in a manifestation of the internal tendency of living creatures to gradually improve. Henry Fairfield Osborn (1857–1935) called the tendency of organisms to improve aristogenesis, while Pierre Teilhard de Chardin (1881–1955) spoke of moving towards the Omega point in the same context. These, in normal terminology, finalistic and, in some cases, directly theistic concepts were more likely to attract the attention of both humanitarian scientists and the general public. Consequently, at the present time, we have a tendency to automatically connect orthogenesis with some of these idealistically oriented concepts. However, in actual fact, most orthogenetic concepts were materialistically oriented and assumed that evolutionary trends arose through the action of normal physical or chemical processes occurring during orthogenesis In the 19th century, Galton already presented a very illustrative mechanical model of orthogenesis (Fig. XXVI.10). The model was based on comparison of the movement of a bead and an irregular polyhedron over a flat surface through the action of external forces. The bead moves strictly in dependence on the direction and intensity of the forces acting at the particular moment. The evolution of organisms through natural selection would occur in this manner if there were no evolutionary constraints. In contrast, for a polyhedron, the direction and rate of movement will be determined both by the direction and intensity of the external forces and also the shape of the body. The polyhedron will not react at all to the action of forces in a certain direction because, in order for it to roll in a certain direction, it must first lift up its centre of gravity, while it will react readily to forces acting in a different direction. A polyhedron is a model for an organism with evolutionary constraints. Such an organism reacts selectively to selection pressures acting in various directions. It need not react at all to a selection pressure acting in a certain direction, while it will react very readily to other selection pressures. In a certain direction, it can even evolve as a consequence of the action of random processes (mutagenesis, drift), i.e. in the absence of natural selection.
            Classical Neodarwinism has a substantial tendency to doubt the importance of evolutionary (and other) constraints in evolutionary processes, i.e. also in the occurrence of evolutionary trends. However, a large portion of evolutionary biologists did not adopt this attitude for substantive reasons, but rather because of the general tendency of Neodarwinists to prefer evolutionary mechanisms including natural selection – i.e. a mechanism that biologists understand and are able to model, in contrast to the complicated and divergent processes of ontogenesis.

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Evolutionary constraints hypothesis of maintenance of sexuality

The existence of evolutionary constraints could be the cause of the preservation of sexual reproduction. Although it could provide a sort of evolutionary advantage for the organism, the transition from sexual reproduction to asexual reproduction in such a complicated organism as a mammal or bird would require such fundamental and extensive changes in the physiology and anatomy that the probability of their occurrence is negligibly small. A less drastic variant of this hypothesis points out the fact that, while the transition to parthenogenesis is, in principle, possible, this would be such a drastic intervention in the physiology of the organism that the parthenogenetic individuals would necessarily have substantially reduced viability and fertility compared to the other members of the population for a great many generations (Uyenoyama 1984).

            The existence of a great many parthenogenetically reproducing species in such complicated organisms as reptiles, amphibians or fish, however, indicates that evolutionary constraints will probably not be the main reason for preservation of sexuality in the vast majority of species.

 

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Evolutionary dissolution of a parasite

see vertical transmission of parasites and virulence

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Evolutionary rates

There is a very obvious inverse dependence between the length of a time period in which the rate of evolution of a quantitative trait is measured and the measured rate of the corresponding evolutionary changes. If we measure the rate of evolution that occurs during a laboratory experiment, values are obtained that are an order of magnitude larger than when the rate of evolution is measured in long-term observations in the field, and the rates of evolution measured in these observations are again many orders of magnitude greater than the values measured on the basis of studies of paleontological material that include a long period of phylogenesis. There are several explanations for this dependence.
Probably the simplest explanation assumes that frequent changes in the direction of evolution are responsible for the given phenomenon. In a short experiment or in medium-long observations in the field, we catch the species or population in a phase when the action of a particular selection pressure leads means that changes in the particular trait consistently occur in a single direction. However, if our observations cover a longer time interval, which is generally true in the study of paleontological material, the species or phylogenetic lines are gradually exposed to various selection pressures that are frequently contradictory from the viewpoint of the monitored trait. Thus, this trait alternately increases and decreases, so that the resultant rate of change in its size over the entire monitored period is necessarily smaller.
Other explanations are based on the fact that, as a consequence of the existence of various evolutionary limitations, any structure can change at a high rate for only a short period of time, while it can change at a low rate over a longer time. For example, if humans were to increase in size by a single millimetre from one generation to the next, i.e. about every 20 years, they would be over 50 metres tall after a million years. It is quite obvious that even a growth rate of 1 millimetre per generation is too large for humans to change size at this rate for a period of a million years. Simultaneously, such a rate is too small for us to be able to register and measure in a laboratory experiment. It is quite logical that laboratory experiments or observations in the field will provide information on evolutionary changes that are fast enough to be registered, while the paleontological record contains information in changes that are sufficiently slow that they can occur over a sufficiently long time.
Another explanation of this phenomenon is based on the idea that the microevolutionary changes studied in experiments or in the field are of a different nature than actual evolutionary changes, which are encountered only in the paleontological record. While microevolutionary changes are based on selection of alleles that were already present in the population beforehand or in the species in the form of intrapopulation or intraspecies variability, macroevolution must wait for the formation of new genetic variants, for new mutations. This idea is also supported by the results of medium-long genetic experiments demonstrating that the rate of change of the relevant selected trait generally decreases gradually during the selection experiment until, after a certain time, the population ceases to respond evolutionarily to the given selection pressure (Fig. XXVI.7). These results are sometimes interpreted in that, during the first phase of the selection experiment, the genetic variability in the population is exhausted and further evolution of the trait is limited by waiting for a new mutation. This simple explanation is, however, most probably erroneous and the retardation or even stopping of evolution is more probably caused by genetic homeostasis (see IV.9.2).
It is apparent that none of the above mechanisms can, in itself, explain the negative correlation between the rate of evolution of a quantitative trait and the length of the time interval during which the particular evolutionary process is monitored, observed on all time scales. However, all of these mechanisms can operate simultaneously and can jointly explain the existence of this correlation very well.

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Evolutionary stasis

Most species that we know from the paleontological record existed for the order of a million to several million years. It is very striking how little the phenotype of a species changes during its existence. While species change during their existence cyclically or acyclically, phenotype changes rarely exceed the limits of normal intraspecies variability estimated on the basis of inter-population differences. It is only thanks to this lack of variability that the geological science known as biostratigraphy can exist. In the biostratigraphic determination of the age of rocks, the existence of evolutionary stasis makes it impossible to utilize changes in the phenotype of individuals occurring within a certain species over time. However, it makes it much easier to utilize changes in the numbers of the individual (phenotype-invariable) species in the particular geological layers (Gould 2002).
Simultaneously, the phenotypes of species remains unchanged even when there is a drastic change in the climate in the region and thus at a time when they are exposed to substantial changes in selection pressures. In fact, it even seems that species change most slowly at the time of the most drastic climate changes, for example at the time of alternation of glacial and interglacial periods (Erwin 2000). If the phenotype of a species changes, then these changes are related primarily to traits that react directly to the physical conditions in the environment of the particular individual, i.e., for example, a change in body weight and overall body dimensions. Most of the changes observed during the existence of a species thus most probably correspond to ecophenotype changes, i.e. changes of a nongenetic nature.
            A period in which no anagenetic processes occur in a particular species is termed evolutionary stasis. Evolutionary stasis is apparently not only a consequence of the absence of selection pressures and the absence of evolution, but is rather a certain type of active evolutionary process. Even in the complete absence of selection pressures, the average phenotype of the members of a certain species should have fluctuated through the action of random processes (e.g. drift) more than they actually fluctuated, as is apparent from the paleontological record. Thus, with great probability, evolutionary forces act on species and their populations, making them resistant to random changes, to be more exact determining the tendency of the population or species to the to the original phenotype after a random change. This force could, for example, be normalization selection. However, because the species retains its typical phenotype even at times of substantial climate changes and over its entire area of occurrence with heterogeneous natural conditions, this explanation is not sufficient.

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Evolutionary synthesis

see History of evolutionism - neo-Darwinist period

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Evolutionary systematists

Evolutionary systematists use the achieved level of anagenesis as the main guideline in defining taxa. If some substantial change in phenotype properties, an important evolutionary innovation, occurred in a certain phylogenetic line, evolutionary systematists frequently consider it useful to classify this line into a discrete taxon, separate from the other lines (Fig. XXV.4). A decision on whether a particular phenotype change is a sufficiently large innovation for its carriers to deserve to be a separate taxon remains a subjective matter. This means that delimitation of the individual taxa in a natural system is, to a considerable degree, a matter of the subjective decision of taxonomists and subsequently of convention. If he is to strictly respect the requirement on monophyly of the created taxa, a systematist must frequently also include in the particular taxon species or groups of species that do not exhibit the given, from our viewpoint key, property. Some species could have retained the original plesiomorphic form of the particular trait or could even return to this form (Fig. XXV.5). A further complication is entailed in the very real possibility that the evolutionary innovation that is to form the basis for defining the taxon could appear independently several times in a phylogenetic line and that this does not correspond to homology but rather homoplasy. It is prohibited to define a taxon on the basis of shared homoplasy; however, it is not clear whether this can always be completely avoided. In some cases, a particular trait is formed on the basis of some other trait functioning as preadaptation for its formation. Consequently, the relevant new features occur within the particular line independently in a number of species whose common ancestor did not exhibit the particular new trait (Fig. XXV.6). In this case, a solution could lie in defining the particular taxon on the basis of the presence of a certain preadaptation; however, it is primarily necessary to consider whether the defining of a taxon on the basis of this trait is at all useful.

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Evolutionary systematists and cladists systems

Evolutionary systematists took a formalized Linnaean system of taxa at various levels, including their nomenclature, from their structuralistically oriented predecessors. They differentiated the originally hierarchical system of organisms into the lowest super-species level of the genus and then gradually into the family, order, class and phylum. As this number of hierarchical levels (ranks) was insufficient for some evolutionary lines, further levels were gradually introduced; for example supplementary categories were created by adding the prefixes sub-, super- and infra- and thus, for example, subgenuses, subfamilies, infrafamilies, superfamilies, and additional categories, for example tribes and cohorts. Basically, it is a matter of convention which taxonomic levels are differentiated for the individual taxon. For example, it is certainly not possible to compare taxa at the same level that belong to different groups of organisms, such as the families of crustaceans and families of birds, on the basis of their evolutionary age or degree of mutual phenotype similarity of their members. In the past, attempts were made to determine the level of a taxon on the basis of its evolutionary age, but this approach has not become established.
            Cladists were forced by objective circumstances to abandon the system of formal taxonomic ranks. As they attempted to create a system of strictly monophyletic taxa (see below), the number of taxonomic levels increased disproportionately, so that it was no longer possible to introduce separate names for them. Consequently, cladists mostly restrict themselves to expressing the rank of a taxon by a number or graphically, by placing (offsetting) the relevant name of the taxon (in cladistic terminology, clad) on the page. They do not attempt to classify the created clads into predetermined categories according to their taxonomic rank. Consequently, evolutionary taxonomists sometimes (pejoratively) call their work, not classification but rather cladification. The cladistic system is less illustrative and less didactic, but contains all the information obtained on the cladogenesis of the studied evolutionary line.

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Evolutionary trap

Biological evolution is basically an opportunist process that cannot predict, in advance, the future effects that a certain change will bring in time. As a consequence, organisms can sometimes end up in a sort of evolutionary trap; structures or patterns of behaviour can emerge and prevail in them that are very detrimental for their carriers and the species. The evolutionary trap mechanism is also sometimes considered to be a possible cause of the present-day predominance of  sexually reproducing species.

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Evolutionary trap hypothesis of maintenance of sexuality

In sexual reproduction, the accumulation of a large number of lethal or more or less semi-lethal recessive alleles can represent an evolutionary trap; these alleles occur with low frequency in the gene pool of every diploid organism but cannot accumulate in haploid organisms. These mutations are active only in the homozygote or hemizygote state and thus are not very influential in an outbred population. However, as soon as a diploid organism begins to reproduce asexually, its offspring become homozygote in the given recessive lethal and semi-lethal genes, which results, at the very least, in reduction of their fitness. Consequently, only a small percentage of mutants can go back from sexual reproduction to asexual reproduction. Transition from asexual reproduction to sexual reproduction (permitting the persistence and accumulation of recessive lethal mutations), similar to transition from haploidy to diploidy, can be a one-way route for more complex organisms, a sort of evolutionary trap, in which most species of organisms finally end up (Bernstein et al. 1985; Crow 1994).

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Exaptations

Exaptations are useful biological structures or patterns of behaviour that developed in a different selection context than that in which they are now advantageous. See alsoPreadaptations.

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Excesive secondary sexual traits

The action of environmental selection can lead to the formation of structures or patterns of behavior with a positive adaptive value, i.e. those that either directly or indirectly improve the chances of survival of organisms in their natural environment. In contrast, the action of sexual selection can lead to structures or patterns of behavior that are detrimental for their bearers, i.e. reduce their viability {10856}.
            The extremely long feathers in the cocks of argus pheasants (Argusianus
argus), which apparently greatly hinder their bearers in flying and moving over the ground, are frequently mentioned as an example. The about 40 kg antlers of the Pleistocene elk Megaloceros giganteus constitute another frequently mentioned example. With a span of 3.5 meters, this weapon for combat between males represented a considerable burden for their bearers, either as a mechanical obstacle to motion in the natural terrain or as a weight that the males had to constantly drag around, and also as the amount of organic matter that they had to grow each year. This example is now frequently thrown into doubt - Megaloceros lived in a landscape without forests and the size of its antlers related to its overall body weight was not greater than that of the other members of the deer species, etc. (Gould 1974). However, a definitive answer to such questions could only be provided by an experiment comparing the rate of growth of a population of elks with antlers and without antlers occurring under otherwise identical conditions. 
            However, the viability of individuals need not be reduced only by hypertrophic body structure. Males could also live to a lower age because of brighter coloring, which increases the risk of attack by a predator. Probably for this reason, secondary sex traits are expressed in some species only at the time of reproduction.
            It has been observed amongst extinct mammals that the length of existence of a species is negatively correlated with the body size of the individual species. Simultaneously, some authors are of the opinion that the main evolutionary motor for an increase in body dimensions in mammals lies just in sexual selection (Mclain 1993). It has been observed for birds artificially introduced on individual islands that the probability of successful introduction is substantially lower for species with sexual dimorphism than for species without marked sexual dimorphism (Mclain, Moulton, & Redfearn 1995). Newer studies performed on North American birds have shown that species with greater sexual dimorphism, to be more exact dichromatism (differences in coloration of males and females) more readily become locally extinct (Doherty et al. 2003).
            The disadvantageousness of some traits acquired through sexual selection has also been observed in intraspecific comparative studies. For example, it has been found that the sexually most attractive guppy males have the lowest viability (Brooks 2000; Godin & McDonough 2003) (Fig. XV.2). However, the results of meta-analyses have shown that the degree of expression of secondary sexual traits is generally positively correlated with the viability of males (Jennions, Moller, & Petrie 2001). This result can have a number of causes. To begin with, the degree of expression of sexual traits can be determined directly by the fitness of the males, so that only extremely fit males can allow themselves to form more obvious secondary sexual traits. In addition, in other species, the formation of secondary sexual traits need not be influenced by the fitness of the individual, but this fitness can fundamentally affect the probability of whether males with extremely accentuated secondary sexual traits survive in nature and whether they can be included in comparative studies.s 

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Excessive traits

The existence of evolutionary trends has often even used to explain the empirically not very substantiated but, in the past, generally accepted fact that some changes occurring in accordance with an existing trend can, in an evolutionarily younger species, even lead to the emergence of excessive traits, i.e. traits whose presence negatively affects the fitness of the individual and, apparently, can lead to the extinction of the particular species or even the entire phylogenetic line. The emergence of extremely large antlers in the giant Pleistocene deer Megaloceros giganteus is a textbook example of such negative consequences of an evolutionary trend. It was long thought that these deer (called Irish elk in older texts) became extinct because an evolutionary trend led to such an increase in the size of their antlers that they prevented movement in a forested landscape. In actual fact the reasons for this extinction were different and the size of its antlers very exactly corresponded to the size of the antlers that an elk of this size should have (Gould 1974). The size of antlers does not increase linearly with an increase in body size but rather faster. This phenomenon is termed growth allometry and is valid to a greater or lesser degree for all body organs in all species of organisms (Fig. XXVI.11). The dependence of a change in organ size (y) on changes in the size of the body (or some other organ) (x) is described by the allometric equation, which is generally written in the form
 

 
where a, b and k are constants characteristic for the particular organ of the given species or the phylogenetic line. Changes in the relevant constants can occur during the phylogenesis of a certain line, so that the character of the allometric dependence can change.
The general existence of growth allometry in a three-dimensional world is basically a logical phenomenon, as the growth of the individual organs and the effectiveness of their functioning can be limited in some cases by their area, in other cases by their cross-section and in still other cases by their weight or volume. Thus, when the body dimensions of an organism increase, it is almost impossible for all the organs and all the morphological structures of the body to increase or decrease in size in direct proportion to the change in body size. If, for example, the radius of the brain were to increase in proportion to the body height, then its volume would increase nonlinearly with the body height (to the third power) so that, for example, the diameter of the veins that would supply it with blood would have to be disproportionately larger than would correspond to a linear increase in body size. In giant deer, there is probably an allometric dependence between the size of the body and of the antlers; put more simply, if the body dimensions of a deer increase by 10%, the head will carry antlers that are 20% heavier. The antler size in deers is not determined by some independent evolutionary trend but rather by selection in the first instance. If there were actually a trend towards an increase in antler size in evolution, then this would most certainly be an enforced trend (Simpson 1961), as a consequence of an increase in the body size of deer species.
            The formation of excessive organs as a manifestation of an evolutionary trend is not considered to be very probable at the present time. Basically, doubt has been thrown on all known textbook examples over time and different explanations have been suggested. The main argument against the existence of this phenomenon consists in the fact that any species whose members are known from the paleontological record was relatively successful in evolution. If a species with a particular excessive trait survived in the environment for a relatively long time, it is strange that the presence of the trait would begin to be detrimental after some time and that it would become extinct. In my view, this argument is not very convincing. The species could become extinct at the time when changes that were incompatible with the presence of the particular trait occurred in the environment. For the giant deer, similar to other large ruminants of the late Pleistocene (woolly rhinoceros, mammoths, etc.), the afforestation of the originally open landscape could have been such a change. In addition, the presence of excessive structures need not, in itself, be the immediate cause of extinction; however, it may mean that a smaller population of the particular species remains in the territory in question. However, this increases the chance that the species could more readily become extinct through a fluctuation in the environmental conditions or the effects of chance. In order to decide whether an evolutionary trend could be the cause of the extinction of a species or phylogenetic line, it would be necessary to perform a series of comparative studies including a greater number of species, and the length of existence of the species with excessive structures and without them would be compared employing, for example, the method of evolutionary contrasts (Harvey & Pagel 1998). Similar studies have been performed for birds and were concerned with traits that were fixed, not by an evolutionary trend, but by sexual selection. It has been found that species with striking secondary sexual traits are actually more susceptible to extinction than species without these traits (Mclain, Moulton, & Sanderson 1999). Understandably, a basic obstacle to performance of similar studies for excessive traits is the means of identification of what is really an excessive trait and what is actually a useful and possibly optimum adaptation to the life style of the particular species. The long teeth of saber-toothed tigers were also long considered to be an excessive trait formed as a result of a “blind” evolutionary trend. In actual fact, this was a useful adaptation for killing large prey; saber teeth emerged at least four times during evolution and the relevant phylogenetic lines were evolutionarily quite successful, i.e. existed for a long time in nature (Gould 2002).

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Exchange of parental roles and sexual selection

It follows from theoretical models and empirical data that more intense sexual selection acts on the members of the sex for which the dependence of the number of fertilized offspring on the number of sexual contacts has the greatest slope, i.e. on the sex exhibiting the steepest Bateman gradient (Andersson & Iwasa 1996) (see Fig. XV.1). The reasons for the steepness of the Bateman gradient can differ for the two sexes. The commonest factor consists in the uneven costs of the production of microgametes and macrogametes (see above). However, there are a number of species of animals for which the two sexes exchange roles and the male invests a greater amount of energy into the production of progeny. In these cases, the male and female frequently also exchange roles in sexual selection; the males are more choosy and more obvious secondary sexual traits appear in the females. The reasons for exchange of parental roles are known in only a few cases.
            Exchange of parental roles occurs relatively frequently in fish. In some species, the male carries the eggs and fry in a special cavity in his body (sea horses); in other cases the male builds a sort of nest in which he cares for the eggs and fry. At the present time, the opinion predominates that exchange of roles occurs in connection with territoriality in males. If a male must fight for and defend a territory, then he invests more in reproduction than the female. In addition, spawning occurs in this territory so the eggs and fry remain in the care of the male.
            Some authors think that exchange of roles in fish could be related to a greater rate of diffusion of milt compared to the diffusion of eggs (Dawkins 1976). This difference means that the male must wait to release the milt into the water until the female releases her eggs. He thus finds himself at a certain disadvantage; at the moment when he fertilizes the eggs, the female can have already left. Consequently, the male must make the choice of whether to care for the embryos and ensure they survive, or to also leave and waste all the expended energy. While it may be advantageous to leave first (the partner must care for the progeny), it is clearly disadvantageous to leave second (there will be no offspring). It is quite possible that the short time that the male must remain at the spawning site after the female could play a decisive role, i.e. can decide who will finally care for the fry. It is good to recall that, in sessile aquatic organisms, the greater rate of diffusion of microgametes means that it is necessary to release microgametes first, where the release of macrogametes is frequently triggered by the presence of microgametes. However, in immobile organisms, the investments into the two types of gametes are the same, the male and female investment into care for progeny is zero and consequently ecological and ethological differentiation of males and females need not occur (Williams 1975).
            Exchanged roles have been observed in insects, for example in some species of water bugs of the Belostomatinae family (Smith 1979). The female lays her eggs on the back of the male and he then carries them, defends them and ensures that they get enough oxygen for about three weeks. The total number of eggs corresponds to twice the weight of the male and care for them is a substantial burden for him. Females can copulate with a number of males, but a male decides whether he will accept eggs from a female or not. As the area of the backs of males is a factor limiting reproduction, fierce competition occurs amongst females for males willing to accept batches of eggs.

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Extended phenotype concept

Most genes apparently affect the probability of their evolutionary fixation in that, through controlling the progress of ontogenesis, they determine the properties and behavior (phenotype) of the individuals in whose genome they are located. As control of ontogenesis is directly or indirectly affected by tens of thousands of genes contained in the genome of the particular organism, the individual genes must learn during evolution to closely cooperate in very varied ways. A great many genes participate in the creation of the final phenotype of an organism in that they affect the expression of other genes, both directly at the level of regulation of gene expression in the nucleus and also indirectly in that, at a certain phase in ontogenesis or the life cycle they affect the probability with which the organisms or certain of their cells encounter inducers or repressors of expression of other genes. If close coevolution of two species of organisms occurs in nature, the individual genes can evolutionarily “learn” to indirectly affect, not only the function of other genes in their own genome, but also the function of genes located in the genome of their coevolutionary partners/competitors. In some cases, these interventions into the creation of the phenotype of a member of a foreign species are facilitated in that both species are, at least temporarily, in close physical contact. In this case, the gene can control the production of a certain product, which can either freely diffuse as the usual morphogen controlling normal morphogenesis into the tissue of the other species, or it can be actively transferred to the relevant tissue (or relevant plant tissue). For example, gall-flies or some kinds of greenfly are capable of using this means to induce the formation of galls on plants, i.e. frequently very complicated bodies formed from the plant tissue, acting as a shelter and often also as a source of food for them.
In other cases, one of the partners directly modifies the genome of the other partner by incorporating some of its genes into it, which then modify the phenotype of one organism to the needs of the second organism. A well-known example consists in the bacteria Agrobacterium tumefaciens, which incorporate their Ti-plasmid into the cells of their plant host; amongst other things, this Ti-plasmid also carries the genes for synthesis of opines, substances that Agrobacterium, as one of the few organisms on Earth, can use as a source of energy (Kado 1998).
However, in a number of cases, one organism affects another organism without actually transferring any substance to it. Rather, it simply passes on information that affects the behavior or properties of the other organism. Of course, this information can be transferred only through a signal and each signal has some material carrier. On the other hand, there is a clear difference between whether one organism affects another through the transfer of genes into its cells or through an optical signal that, after evaluation by the nervous system of the recipient, initiates a certain pattern of behavior in the second organism. The close evolution of pairs of species can thus lead to a situation where the phenotype of one organism, and thus some of its traits, i.e. properties or patterns of behavior, are controlled by genes that are located in the genome of the organism of a different species. In these cases, the particular traits are frequently disadvantageous for their carrier and simultaneously advantageous for the organism in whose genome they are coded. Consequently, not only those alleles that usefully affect, from their viewpoint (i.e. from the viewpoint of the effectiveness of their own reproduction), the phenotype of the individuals in whose genome they are located, but also those alleles that thus affect the phenotype of other individuals, including the phenotype of the members of another species, can become fixed in evolution. In these cases, we say that certain genes control (affect) the creation of an extended phenotype, i.e. a phenotype that is not limited by the physical boundaries of the individual in whose genome the particular genes are located (Dawkins 1982).
It is apparent that the phenotype of a certain individual can be more easily affected by its own genes than by the genes that are located, for example, in the individuals of another species. If some foreign genes “attempt to modify” the phenotype of an individual contrary to the interests of its own genes, those alleles that will prevent the foreign genes in their phenotype manifestations (in manipulation) will become fixed in the manipulated species during coevolution. The outcome of the coevolutionary battle between the species, however, depends on a number of factors (see also XIX.1). To begin with, any difference in the intensities of the selection pressures acting on the manipulated and manipulating species will be important here. Fixation of the particular manipulating gene will be more probable if successful manipulation is a necessary precondition for reproduction of the manipulating species and thus for the transfer of the manipulating alleles to the next generation. It is also more probable if the submission to manipulation will not substantially reduce the fitness of the manipulated individual. Similarly, the manipulators will have an advantage over the manipulated species if biological evolution occurs faster or more effectively in it for some reason. A basis for faster evolution of the manipulators than in the manipulated species can, for example, consist in a shorter generation time or greater number of progeny (see XIX.1.1) in the manipulators.
The members of nonreproducing casts in eusocial species become an object of manipulation especially easily. The nests of ants and bees contain an enormous number of species of organisms whose members parasitize on their hosts and allow themselves to be fed by them, be moved from one place to another and have their progeny cared for by them. These social parasites induce the relevant behavior, advantageous for the parasite, in the host workers through specific chemical, tactile or optical signals. The easy manipulation of the members of sterile casts in eusocial species is caused by the fact that individual selection cannot be active amongst them. The workers of ants that do not submit to manipulation have no evolutionary advantage compared to workers that submit to manipulation. Selection in the direction of resistance to manipulation can occur only at the level of the individual colonies and thus with far lower effectiveness than in the parasitic species. It is apparent that, in eusocial species, their manipulability can also be assisted to a substantial degree by the fact that the individuals already exhibit a number of patterns of behavior connected with care for the members of their own nest and that it is sufficient for the parasitizing species to simply evolutionarily learn to induce these patterns in situations advantageous for it through the relevant initiation signal.

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Extinction predispositions

As was already mentioned in the part dealing with mass extinction, the members of certain groups of organisms were affected more by extinction in the individual periods of the history of the Earth. The sensitivity of the individual groups differed in the various cases, apparently in dependence on the immediate cause of the particular mass extinction. However, irregardless of the cause of the particular mass extinction, certain long-term trends and long-term patterns can be seen in the sensitivities of the members of the individual groups of organisms to extinction. In general, it can be stated that the probable length of existence of a species differs substantially in dependence on its taxonomic affiliation and its life style. Marine species of mussels and snails exist for an average of 10 – 20 million years. In contrast, the average lengths of the lives of mammal species are far shorter, generally substantially less than 5 million years. Amongst marine invertebrates, plankton species have shorter lifetimes than benthic species. If we ignore the theoretical possibility that a great many extinctions actually correspond to pseudo-extinctions and that the rates of extinctions actually correspond to the differences in the rates of anagenesis or even the convention of taxonomists dealing with the particular group of organisms, the main reason for these differences lies in the unequal probability of extinction of species within the individual groups of organisms. As the most intense competition can be expected for mutually closely related species, it is probable that the frequency of extinction can also be increased by increased frequency of speciation. According to some authors, the very fact that a certain species splits off a daughter species substantially increases the probability of its extinction (Pearson 1998) {5302}. In relation to the duration of existence of higher taxa, on the other hand, the species abundance of the taxon will reduce the probability of its extinction and taxa including a greater number of species will, on an average, exist for a longer time.
            The individual species differ in the width of their ecological valence. Eurytopic species are capable of utilizing a wider range of resources and successfully surviving in various types of habitats; in contrast, stenotopic species specialize on a narrow range of resources and are capable of surviving only in a narrow range of conditions. Comparative studies have shown that stenotopic species have a far greater tendency to become extinct than eurytopic species (Purvis, Jones, & Mace 2000). This is undoubtedly a result of the fact that eurytopic species are capable, when necessary, of reorienting themselves to a different type of resource, are capable of tolerating quite drastic climatic changes and generally occur over a broader area than stenotopic species. As will be mentioned below (XXII.6.3), the size of the geographic range tends to be the decisive factor from the viewpoint of survival of the species.
 
            At least in some cases, physical proportions affect the probability of survival of a species; specifically they are negatively correlated with the length of existence of a species (Raup 1994). However it is probable that the lower rate of reproduction of large species is important here. This dependence was quite apparent in the Late Pleistocene, although the causes were rather atypical. At that time, primarily large mammals and birds became extinct, specifically species weighing more than 44 kg (Gittleman & Gompper 2001). These species became extinct almost all around the planet over a very short period of time. Simultaneously, this extinction occurred at different times in the individual parts of the world. For example, in North America, this extinction event lasted approximately 200 years, in a period about 10,800 to 11,000 years ago, during which 72% of large animal species and only 10% of small animal species became extinct. This selective extinction was greatest in South and North America, Australia and Madagascar, while Africa and Asia were affected far less. The most probable cause of this extinction, which is also termed Blitzkrieg extinction, was hunting of large animals by humans. The time of disappearance of animals at the individual places correlated very well with the arrival of humans in this territory. The extinction was not so marked in places where settlement occurred gradually or where humans had lived from the very beginning, as the animals apparently had time to adapt to this dangerous predator; in contrast, the extinction was greater in territories that were settled rapidly.
            Greater sensitivity of large animals to extinction was also manifested at other times. It is highly probable that it could be connected with the relatively smaller sizes of the populations of larger organisms. The resistance to extinction is positively correlated with the size of the population and is thus negatively correlated with the size of the members of a particular species.

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Extinction, viral theory of background extinction

While the presence of a planktonic larval stage in the life cycle reduces the probability of extinction, the planktonic life style of adults, which is generally connected with the formation of extensive mutually interrelated populations, is, on the other hand, connected with a greater tendency towards background extinction. It has been found for Foraminifera that planktonic species exist an average of 7 million years, while benthic species exist for an average of 20 million years (Emiliani 1993).
This could be explained by the viral theory of background extinction. Detailed analysis of paleontological data indicates that, while larger groups of species become extinct at once at some moments, frequently accompanied by a temporary decrease in the size of the populations of other species, at other times only extinction of individual species occurs and the other species occurring at the same time in the same environment remain practically untouched by extinction. In the former case, the cause of simultaneous extinction of several species could lie in sudden changes in the environment. It is difficult to find a possible explanation for the second type of extinction, i.e. for selective extinction that affects only one species. There are very few factors in the environment that are so specific that they are capable of destroying only one species and not affecting other species.
One of the considered possibilities is a pandemic caused by a parasitic organism, most probably a virus. A number of parasites, including viruses, have absolute host specificity, so that they attack and destroy only the members of a single species (Emiliani 1993). Viruses occur in very high concentrations in a marine environment, in numbers from millions to billions of viral particles per mm3 of water. It is assumed that they have a fundamental effect in regulating the population size of individual species and thus on ecological interspecies interactions. Some authors are of the opinion that, from time to time, a lethal viral variant can emerge against which the host species cannot defend itself and that can therefore spread uncontrollably throughout the entire population of this species and thus cause its extinction. From the viewpoint of theoretical parasitology, this phenomenon is possible but can occur only under very specific conditions (see XIX.1.4). In most cases, the parasite dies out before it can manage to exterminate its host. The effectiveness of the transmission of the infection from host to host generally decreases with decreasing density of the host population, and as soon as the actual reproduction rate of the parasite decreases below a value of 1, i.e. as soon as one infected host infects an average of less than one uninfected host, the epidemic comes to an end. Even if the parasite initially exhibits great virulence and kills a great many infected hosts, the virulence in the population will most probably gradually decrease over time to a value that corresponds to its maximum basic reproduction rate (see XIX.4). However, a different situation can occur if the parasite forms resistant stages that are capable of surviving in the environment even for a long time after they are released from an infected host. In this case, a delay occurs in the parasite-host system, so that the number of infected individuals increases even after a decrease in the size of the host population. This can lead to progressively increasing oscillations that can result in a decrease in the numbers of the host population to zero.
Parasites with several or even many alternative host species can also exterminate a host. These parasites can survive for a long time in the population of a certain species without in any way harming this species. Simultaneously, they can completely eliminate the population of some other species. A well-known contemporary example is the helminth Parelaphostrongylus tenuis, which does not basically harm its natural host, the white-tailed deer (Odocoileus virginianus) but causes very serious diseases in the members of other deer and elk species. Because of this parasite, no other species of deer or elk are found in areas where white-tailed deer occur.
Species forming dense, spatially unstructured populations would apparently be exposed to a greater risk of extermination by a parasite than species forming equally large, but less dense, spatially structured populations. Planktonic species are typical examples of the former kind, while the latter kind tends to be found amongst benthic species.
The contribution of a viral epidemic could also explain the partial taxonomic specificity of some waves of extinction. A great many viruses have a broader host spectrum and can attack a greater range of phylogenetically related species. In contrast to the situation related to most abiotic factors, the risk of infection as well as the sensitivity of the individual species to the negative action of a parasite could actually be correlated with their phylogenetic relatedness rather than with the similarity of their ecological niches.
The important role of parasitic organisms in the extinction of species was also confirmed for some extinctions observed in recent times. It is assumed that this was important for some species of birds in Hawaii, the Tasmanian tiger, and a number of species of snails of the Partula genus. At the present time, a great many species of amphibians seem to be dying out as a consequence of a pandemic of parasitic chytridiomycota (Daszak & Cunningham 1999).

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Extinctions

Most of the species that ever existed on the Earth became extinct at some time in the past. It has been estimated that the number of species existing at the present time corresponds to the order of one per mille to one percent of the number of extinct species (Raup 1994). It is rather difficult to perform a more exact quantitative estimate as the probability that a certain species will be found in the paleontological record is directly proportional to the duration of its existence. It is thus apparent that the major part of preserved fossils will correspond to species that survived for a sufficiently long time on the Earth and, to the contrary, we will learn nothing from the paleontological record about the existence of short-lived species. Similarly, it is obvious that a great many of the traits, on the basis of which modern species are distinguished within a certain taxon, are apparent only on the soft parts of their bodies and were thus not preserved in fossils. Nonetheless, the paleontological data clearly demonstrate that species are formed at a certain moment, survive for a longer or shorter time and finally disappear, become extinct. The situation is similar for higher taxa – however, they understandably exist far longer than individual species and become extinct only when their last members become extinct.
            At a general level, the most common cause of extinction of a species is “bad luck”, the fact that it was present at the wrong time in the wrong place. Losing the coevolutionary battle with another species apparently occurs far less often. It seems that, at the very least for tetrapod vertebrates, new species mostly expanded into a previously vacated ecological space (Benton 1996). Apparently the vast majority of extinctions occurred in that, at a certain moment, the species was suddenly exposed to conditions that it had not encountered in the past and to which it was thus not adapted. Of course, amongst other things, this means that it is not species and developmental lines that were best able to adapt to the current conditions in their environments that survive for long times, but rather species and evolutionary lines that were fortunately able to survive in situations that they had never encountered before. Thus, paleontologists often point out the contrast between microevolution, based on survival of the fittest, and macroevolution, based rather on survival of the luckiest. Obviously, the degree to which this sharp division corresponds to facts could be a matter for long discussions. In any case, compared to microevolutionary processes, luck certainly plays a much greater role in macroevolution (Raup 1994).
            A species become extinct when all its members die. Higher taxa become extinct when all the species that they encompass become extinct. The basic model of extinction assumes that the individual species become extinct independently of one another. If, for example, ten taxa at the highest level are considered, of which each can be divided into ten taxa at the central level and each of these taxa contains ten species then, for example, if, during a certain period in which speciation does not occur, 90% of species die at random, simultaneously 35% of taxa at the central level become extinct and probably only 0.003% of taxa at the highest level (i.e. in this case, probably none). More realistic models, which consider unequal numbers of species and taxa in various taxa at the same level, yield somewhat different numbers, but the results are basically similar.
For example, the number of species that became extinct during the greatest known mass extinction 248 million years ago at the end of the Permian has been estimated by the method of reverse rarefication on the basis of the number of extinct genera and families on the actual distribution of species in the individual taxa as 96% (the newest estimates yield somewhat lower values). The model describing the extinction of higher taxa on the basis of the independent random extinction of their individual species is called the foot soldier in the field model. Even if 90% of foot soldiers were shot and killed, most probably “only” 35% of ten-membered squadrons would be killed, only about 4% of platoons consisting of 3 squadrons and only about 0.008% of troops consisting of 3 platoons, etc. It is apparent that such a model would not apply to a real battle. Either the individual troops and their platoons wouldn’t all attack at once and be mixed up, but in a certain order, or, for example, some of the members of each formation would be left behind somewhere and would most probably survive. In the former case, more of them would be wiped out while, in the second case, fewer higher formations (higher taxa) would disappear than would correspond to the number of dead foot soldiers.
            Study of paleontological material demonstrates that, even for the extinction of higher taxa, the foot soldier in the field model does not adequately describe the real situation. For example, it is improbable that all the taxa of the numerous and extremely diversified trilobite taxon could have died in the Paleozoic or that both orders of dinosaurs (Saurischia and Ornithischia) would have become extinct at the end of the Mesozoic. It is apparent that, at least in some periods of the history of life, membership in a taxon affected which species would become extinct and which would survive. However, the foot soldier in the field model is an extremely useful instrument from the methodological point of view as it represents the zero hypothesis against which other more complicated and more realistic models can be tested.

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Extinctions contemporary

At the present time, extremely intensive extinction of organisms is occurring around the world as a consequence of human activity and the increase in the abundance of human populations. It has been estimated that the contemporary extinction rate is approximately 1000 times greater than the usual rate of background extinction (Novacek & Cleland 2001). This extinction is not, at first glance, obvious, because only a small percentage of known endangered fauna have so far become extinct. However, the vast majority of species of organisms on the Earth consist of arthropods and helminths living in the tropics, the greater majority of which have not yet even been named. Because of the destruction of natural habitats, especially tropical rain forests, 30% of these species will become extinct to the middle of this century, i.e. only slightly less than 30% of all species. The extent and rate of contemporary extinctions are thus approaching those of mass extinction. It is encouraging that the 30% reduction in diversity will apparently not be accompanied by a 30% reduction in disparity, as the number of basic types of body structure will apparently be preserved, although quite probably as a result of the efforts of zoological gardens and reservations. On the other hand, it is discouraging that, in contrast to all the former periods of mass extinctions, following which the original biodiversity was renewed with a certain delay, something similar will apparently not occur in this case. Humans not only exterminate species but primarily irreversibly take over their environment. This means that nature will have to wait until the period following the next successful mass extinction for renewal of the original biodiversity. Unfortunately, if the mass extinction is to be “successful”, members of our species will not be able to enjoy the renewed biodiversity.

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Extinctions types

Species became extinct throughout all the periods in the history of the Earth. However, relatively few species become extinct in some periods while, at other times, the rate of extinction, i.e. the number of species that became extinct over a certain time interval, temporarily increased drastically (Fig. XXII.2.). On the basis of Sepkoski’s database of 17,621 genera of marine fauna, it has been estimated that the average risk of extinction of a species is 0.25 per million years. However, this value was calculated as an average of the negligible risk of extinction over long periods of time and the very high risk during other periods (Raup 1991). In some periods, the majority of existing species became extinct almost at a single instant, so that even entire higher taxa died out. Extinction is usually classified as mass extinction and “normal” extinction, which is usually termed background extinction. Sometimes, only the “big five” extinctions are classified in the category of mass extinctions, i.e. extinctions at the end of the Ordovician, in the later Devonian, at the end of the Permian, Triassic and Cretaceous (Fig. XXII.3). Simultaneously, some authors do not consider the extinctions before the end of the Devonian and at the end of the Triassic to be real mass extinctions as, in contrast to other periods, the mass extinction was not accompanied by a substantial reduction in the overall biodiversity (Kerr 2001). However, fundamentally, it is highly questionable whether there is actually a difference in principle between mass and background extinction. There were certainly more than five periods with elevated intensity of extinction. In all probability, these periods differed both in the intensity, i.e. number of species affected, and in selectivity. However, there were smooth transitions in both the intensity and selectivity of the extinctions and there were also only rather loose correlations between the selectivities and intensities. For a number of reasons, it is practical to classify extinction as mass and background and thus this will be retained here. However, it is necessarily to constantly bear in mind that the individual periods of extinction always had a specific cause and specific course and that any generalization on the differences between mass and background extinction can hold only under certain conditions.

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Extinctions, macroevolutionary trends

In most organisms, the probability of the death of an individual changes in dependence on their age. In the typical case, the probability of death during a certain time interval is high for very young individuals, low for individuals of middle age and again high and gradually increases for old individuals. Thus, if a group of individuals of a certain age is monitored from a certain moment and the number of individuals from the original group surviving is plotted on a graph at regular intervals, the survival curve will turn sharply down at a certain moment. However, apparently no such dependence of the probability of extinction on the length of existence of the species will be found for the extinction of entire species and the probability of extinction does not depend in any way on the age of the species (Fig. XXII.11). The times of existence of species exhibit an exponential distribution (Fig. XXII.12); thus, if we plot the histogram of the abundance of species in dependence on the length of their existence on a semilogarithmic scale, i.e. the height of the columns in the histogram will correspond to the logarithm of the number of species with different times of existence, a roughly linear dependence will be obtained.
This result, which was first obtained by van Valen (1973), is certainly surprising. To begin with, it overturns the rather naive concept that species, similar to individuals, age as they get older and that they thus have a predetermined limited maximum length of existence. In this case, a curve fitted through the tops of the columns in the histogram would suddenly turn down in the right-hand part; there would be fewer species with long periods of existence. However, what is more important is that the curve does not turn down at all in the right-hand part. This result means that species do not become more resistant to extinction during their existence. As natural selection acts constantly on species and should lead to gradual accumulation of positive mutations, it would be logical to anticipate that the probability of extinction would gradually decrease for each species.
            The absence of relevant correlations between the probability of extinction and the length of existence of a species led van Valen to formulate the red queen hypothesis in the 1970’s. According to this hypothesis, the main factor affecting the survival of a species is the progress of the coevolutionary battle between the particular species and its competitors, its prey and its predators and parasites. As the properties of a certain species improve in evolution, the properties of the other species also improve, so that the result of the evolution of the particular species is only that it keeps pace with the other species forming its niche. Thus, if a species is capable of evolving at the same rate as its competitors, the probability of its survival will not increase but, on the other hand, it will also not decrease.
            The red queen model has been employed in the area of microevolution, as one of the explanations of maintenance of sexuality in the population. However, its applicability to the study of macroevolutionary processes has been problematic. It is not easy to explain why the rate of microevolution of a certain species should be exactly the same as the rate of microevolution of all its opponents. Contemporary models assume that, as soon as a certain species begins to lag behind its opponents, there is an increase in the selection pressure acting on it, increasing the rate of its evolution. However, a problem is encountered in the fact that the ability of evolution to respond to selection pressure of the same strength differs substantially in various species of organisms while, for irreversible loss in the evolutionary battle, i.e. extinction, it is sufficient for the species to lose the battle against a single opponent. However, the fact that, in addition to biotic effects on the species, abiotic effects are also active and the species should gradually escape from their reach through its microevolution.
            An alternative explanation of the absence of a correlation between the probability of extinction and the length of existence of a species is provided by the model of frozen plasticity (Flegr 1998, Flegr 2010). This model assumes that a reproducing sexually species is evolutionarily plastic only immediately following its emergence and cannot react very much to external selection pressures at later times. If this model corresponds to fact, the absence of correlation between the probability of extinction and the length of existence of a species is a quite logical phenomenon.

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Extra-pair copulation

Extra-pair copulation - For a female, an ideal sexual partner should simultaneously be maximally fit, sufficiently sexy and simultaneously willing to invest the greatest possible amount of time and energy into care for his offspring. It follows from the existence of conditional strategies that it is very improbable that such a partner will be found. Thus, the female must decide on some sort of compromise, reducing her demands in one or the other area or must find a suitable counter-strategy.  The most effective strategy according to which the female can resolve problems connected with selection of a sexual partner consists in separation of the roles of care-giver and biological father. She can achieve this shrewd solution in a simple way, which is called extra-pair copulation (EPC) in animals, while we use a commoner term amongst humans – partner infidelity. For females, the optimum state exists when the partner in biparental care for offspring (or even exclusive care for offspring) is the winner in the game for “who is the dumbest”, a male willing to invest the greatest amount into care for his offspring, while the biological father of the greatest number of progeny will be the male with the best combination of viability, fertility and sex-appeal. Direct observations in nature, in combination with modern molecular-biological methods of determining paternity, have shown that, in a large number of species of mammals and birds, females achieve this result with surprisingly high frequency (Sundberg & Dixon 1996), {12659} (Fig. XIV.9).

            It is obvious that a situation that is optimum from the standpoint of the female is disadvantageous from the viewpoint of the male caring for foreign progeny, and thus that the emergence of an appropriate male counter-strategy can be expected. The males mostly try intensely to prevent partner infidelity. They guard the female in the critical period and chase other males out of the territory. In a great many species, the male delays the first copulation to a time when it is obvious that the female has not been previously fertilized by a different male. In other cases, he mechanically prevents entrance into the sexual organs of the female following copulation. For example, some spiders create such a “chastity belt” in that, following copulation, they break off and leave part of their own sex organs in the sex organs of the female. In a great many species of mammals, including those species of primates in which their life style and reproduction strategy make competition of sperm very probable, the sperm coagulate in the female reproductive organs and form a copulation plug (Polak et al. 2001; Baumgardner et al. 1982; Dixson & Anderson 2002).

            A very common counter-strategy, through which the male at least minimizes losses following from partner infidelity, consists in reducing care for those offspring for which there is a greater risk that that they come from foreign fathers. In starlings and warblers, it has been found that the amount of paternal care is directly proportional to the time during which the male had the female “under control” in the critical period (Wright & Cotton 1994; Dixon et al. 1994) (Fig. XIV.10).

            In humans, it has been found that children, according to newer studies only sons, are similar to their fathers, especially in the first years of life, when it could be useful to ensure a suspicious father that the offspring is really his (Christenfeld & Hill 1995) {12874}. It has also been found that fathers, in contrast to mothers, were willing to invest in their children in proportion to how similar these children (on computer-modified photographs) are to them {11457}. Critics of these studies objected that, in prehistoric time, fathers did not have any mirrors, so that they had limited information about their own appearance (Bains 1996). However, it can be assumed with probability bordering on certainty that malicious uncles, aunts and friends were very willing to provide them with the relevant information even in prehistoric times.

            The male can also attempt to increase the probability of his biological paternity by copulating with the female repeatedly and, in some species, with high frequency. Simultaneously, the amount of sperm in the ejaculate is frequently far greater than the theoretical biological requirement. If the female is guilty of only isolated partner infidelity, there is high probability that the less numerous sperm of the foreign male will lose out in competition with the more numerous sperm of the social partner. It is known that, in many taxa, the size of the testicles and thus the number of sperm produced is positively correlated with the probability of repeated copulation of a single female with particular males (Hosken 1997) (Fig.. XIV.11 and Fig. XIV.12). Studies performed on humans (Baker & Bellis 1993a) have also shown that the amount of ejaculate in sexual intercourse is increased with the length of time during which the partners were not together in the previous period (and thus with the probability of partner infidelity and possible sperm competition).

            Thus partner infidelity is extremely advantageous for females for two reasons. On the one hand, it can lead to the optimum result (a male willing to invest the maximum amount of energy in care for progeny will take care of the offspring of a genetically ideal male) and, on the other hand, forces the male to invest substantial efforts in ensuring his biological paternity in the initial stages of reproduction (production of a large number of sperm, guarding the female, etc.), so that this reduces the advantageousness of the male strategy “if not this one, then another one”.

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