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

see Inertia of sexual selection

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.

see History of evolutionism - pre-Darwinist period

see Anagenesis in parasites

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.

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.

See Epigenetic inheritance.

see Reproductive isolation barriers internal

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.

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.

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).

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.

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.

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.

- 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 19^th 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.

see vertical transmission of parasites and virulence

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.

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.

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.

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.

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).

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.

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).

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.

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.