Adaptation and ecological resistance

The notion fitness, widely used in genetics usually serves to measure a relative rate of organism reproduction. Another important character of an organism is its ecological resistance which is basically the product of macroevolution. It can be determined as a probability of an organism survival and participation in reproduction of the species. Ecological resistance determines the level of the accidental death of organisms that are genetically valuable. For the comparison of ecological resistance in different organisms and species the negative meanings of the Malthusian parameter can be used. Ecological resistance depends on the presence in genomes of essential genes and fairly complete sets of nonessential, or adaptive, genes which can reside in genomes both as "plus" and "minus" alleles. The recovery of complete sets of adaptive genes lost as a result of mutations and, thus, of a high level of ecological resistance in organisms is provided by genetic exchange between them. With respect to mutations leading to the increase in fitness the effect of genetic exchange is negative since it leads to the formation of recombination load, i.e. a decrease in fitness of the offspring. In microevolutionary processes, the elevation in ecological resistance level does not take place since it requires a long time for the formation of new genes and new elements of organization in the process of positive selection. At the same time, a constant recovery of a high level of ecological resistance of the species decreased as a result of mutations takes place in some individuals due to genetic exchange. Mutations affecting ecological resistance of an organism, as a rule, cause a decrease in its viability and they are usually excluded from populations as a result of negative (stabilizing) selection.     

The nature of adaptive evolutionary changes: fitness and potential

Ecological potential of an individual can be defined as its viability in the broad sense including the ability to reproduce in various environments. From the biological viewpoint, ecological potential as a fundamental property of an organism is more important than fitness in the genetic sense, which is estimated as the relative rate of reproduction. In essence, fitness reflects the level of implementation of the biological potential. In the process of evolution, regulatory selection results in an increase of fitness: selected forms reproduce more successfully as the population size increases. By contrast, individuals with high ecological potential are more advantageous when the population size decreases, because the probability of their survival in adverse environments is high. Thus, high levels of fitness and ecological potential are achieved via operation of different types of selection.     

The Genetic Explanation of Vertical Evolution

The genetic theory of natural selection proposed by Fisher takes into account differential reproduction success of organisms, which may be estimated by using the Malthusian parameter as fitness. However, the minimum possible value of this parameter depends on ecological stability of an organism, which determines the probability of the survival and participation in reproduction for each viable offspring. In the course of vertical evolution, leading to an increase in the level of biological organization, ecological stability of organisms increases, and this might be accompanied by a decrease in their fitness. In the macroevolutionary process, alterations in ecological stability of organisms, including those responsible for an increase in the level of biological organization, are basic and primary changes whereas alterations in fitness are additional and secondary.     

Genetic explanation for vertical evolution

The genetic theory of natural selection proposed by Fisher takes into account differential reproduction success of organisms, which may be estimated by using the Malthusian parameter as fitness. However, the minimum possible value of this parameter depends on ecological stability of an organism, which determines the probability of the survival and participation in reproduction for each viable offspring. In the course of vertical evolution, leading to an increase in the level of biological organization, ecological stability of organisms increases, and this might be accompanied by a decrease in their fitness. In the macroevolutionary process, alterations in ecological stability of organisms, including those responsible for an increase in the level of biological organization, are basic and primary changes whereas alterations in fitness are additional and secondary.     

The impact of random frequency-dependent mutations on the average population fitness

ABSTRACT: BACKGROUND: In addition to selection, the process of evolution is accompanied by stochastic effects, such as changing environmental conditions, genetic drift and mutations. Commonly it is believed that without genetic drift, advantageous mutations quickly fixate in a halpoid population due to strong selection and lead to a continuous increase of the average fitness. This conclusion is based on the assumption of constant fitness. However, for frequency dependent fitness, where the fitness of an individual depends on the interactions with other individuals in the population, this does not hold. RESULTS: We propose a mathematical model that allows to understand the consequences of random frequency dependent mutations on the dynamics of an infinite large population. The frequencies of different types change according to the replicator equations and the fitness of a mutant is random and frequency dependent. To capture the interactions of different types, we employ a payoff matrix of variable size and thus are able to accommodate an arbitrary number of mutations. We assume that at most one mutant type arises at a time. The payoff entries to describe the mutant type are random variables obeying a probability distribution which is related to the fitness of the parent type. CONCLUSIONS: We show that a random mutant can decrease the average fitness under frequency dependent selection, based on analytical results for two types, and on simulations for n types. Interestingly, in the case of at most two types the probabilities to increase or decrease the average fitness are independent of the concrete probability density function. Instead, they only depend on the probability that the payoff entries of the mutant are larger than the payoff entries of the parent type.     

Elevated temperature increases genome-wide selection on de novo mutations

Adaptation in new environments depends on the amount of genetic variation available for evolution, and the efficacy by which natural selection discriminates among this variation. However, whether some ecological factors reveal more genetic variation, or impose stronger selection pressures than others, is typically not known. Here, we apply the enzyme kinetic theory to show that rising global temperatures are predicted to intensify natural selection throughout the genome by increasing the effects of DNA sequence variation on protein stability. We test this prediction by (i) estimating temperature-dependent fitness effects of induced mutations in seed beetles adapted to ancestral or elevated temperature, and (ii) calculate 100 paired selection estimates on mutations in benign versus stressful environments from unicellular and multicellular organisms. Environmental stress per se did not increase mean selection on de novo mutation, suggesting that the cost of adaptation does not generally increase in new ecological settings to which the organism is maladapted. However, elevated temperature increased the mean strength of selection on genome-wide polymorphism, signified by increases in both mutation load and mutational variance in fitness. These results have important implications for genetic diversity gradients and the rate and repeatability of evolution under climate change.     

Amplicon Remodeling and Genomic Mutations Drive Population Dynamics after Segmental Amplification

New enzymes often evolve by duplication and divergence of genes encoding enzymes with promiscuous activities that have become important in the face of environmental opportunities or challenges. Amplifications that increase the copy number of the gene under selection commonly amplify many surrounding genes. Extra copies of these coamplified genes must be removed, either during or after evolution of a new enzyme. Here we report that amplicon remodeling can begin even before mutations occur in the gene under selection. Amplicon remodeling and mutations elsewhere in the genome that indirectly increase fitness result in complex population dynamics, leading to emergence of clones that have improved fitness by different mechanisms. In this work, one of the two most successful clones had undergone two episodes of amplicon remodeling, leaving only four coamplified genes surrounding the gene under selection. Amplicon remodeling in the other clone resulted in removal of 111 genes from the genome, an acceptable solution under these selection conditions, but one that would certainly impair fitness under other environmental conditions.     

Bacterial evolution through the selective loss of beneficial Genes. Trade-offs in expression involving two loci

The loss of preexisting genes or gene activities during evolution is a major mechanism of ecological specialization. Evolutionary processes that can account for gene loss or inactivation have so far been restricted to one of two mechanisms: direct selection for the loss of gene activities that are disadvantageous under the conditions of selection (i.e., antagonistic pleiotropy) and selection-independent genetic drift of neutral (or nearly neutral) mutations (i.e., mutation accumulation). In this study we demonstrate with an evolved strain of Escherichia coli that a third, distinct mechanism exists by which gene activities can be lost. This selection-dependent mechanism involves the expropriation of one gene's upstream regulatory element by a second gene via a homologous recombination event. Resulting from this genetic exchange is the activation of the second gene and a concomitant inactivation of the first gene. This gene-for-gene expression tradeoff provides a net fitness gain, even if the forfeited activity of the first gene can play a positive role in fitness under the conditions of selection.     

Population waves as a condition for increasing ecological stability of organisms in the process of vertical evolution

Ecological stability of an organism, which determines the possibility of its existence under changing environmental conditions, can be estimated as the probability of the participation of each viable offspring in reproduction. In developing species, the periodic rises and falls in the population size (Chetverikov's "waves of life") can lead to changes in ecological stability, which is of macroevolutionary importance. Under conditions of isolation such changes generally result in specialization of intraspecific races but they could then lead to an increase in ecological stability of hybrid forms. Ecological stability of prosperous species increases during macroevolution due to combinative recombination between specialized intraspecific races or closely related species.     

The genetic architecture of behavioral canalization

Behaviors are components of fitness and contribute to adaptive evolution. Behaviors represent the interactions of an organism with its environment, yet innate behaviors display robustness in the face of environmental change, which we refer to as ‘behavioral canalization’. We hypothesize that positive selection of hub genes of genetic networks stabilizes the genetic architecture for innate behaviors by reducing variation in the expression of interconnected network genes. Robustness of these stabilized networks would be protected from deleterious mutations by purifying selection or suppressing epistasis. We propose that, together with newly emerging favorable mutations, epistatically suppressed mutations can generate a reservoir of cryptic genetic variation that could give rise to decanalization when genetic backgrounds or environmental conditions change to allow behavioral adaptation.     

Compensatory evolution of pbp mutations restores the fitness cost imposed by β-lactam resistance in Streptococcus pneumoniae

The prevalence of antibiotic resistance genes in pathogenic bacteria is a major challenge to treating many infectious diseases. The spread of these genes is driven by the strong selection imposed by the use of antibacterial drugs. However, in the absence of drug selection, antibiotic resistance genes impose a fitness cost, which can be ameliorated by compensatory mutations. In Streptococcus pneumoniae, β-lactam resistance is caused by mutations in three penicillin-binding proteins, PBP1a, PBP2x, and PBP2b, all of which are implicated in cell wall synthesis and the cell division cycle. We found that the fitness cost and cell division defects conferred by pbp2b mutations (as determined by fitness competitive assays in vitro and in vivo and fluorescence microscopy) were fully compensated by the acquisition of pbp2x and pbp1a mutations, apparently by means of an increased stability and a consequent mislocalization of these protein mutants. Thus, these compensatory combinations of pbp mutant alleles resulted in an increase in the level and spectrum of β-lactam resistance. This report describes a direct correlation between antibiotic resistance increase and fitness cost compensation, both caused by the same gene mutations acquired by horizontal transfer. The clinical origin of the pbp mutations suggests that this intergenic compensatory process is involved in the persistence of β-lactam resistance among circulating strains. We propose that this compensatory mechanism is relevant for β-lactam resistance evolution in Streptococcus pneumoniae.     

The experimental evolution of herbicide resistance in Chlamydomonas reinhardtii results in a positive correlation between fitness in the presence and absence of herbicides

Pleiotropic fitness trade-offs will be key determinants of the evolutionary dynamics of selection for pesticide resistance. However, for herbicide resistance, empirical support for a fitness cost of resistance is mixed, and it is therefore also questionable what further ecological trade-offs can be assumed to apply to herbicide resistance. Here, we test the existence of trade-offs by experimentally evolving herbicide resistance in Chlamydomonas reinhardtii. Although fitness costs are detected for all herbicides, we find that, counterintuitively, the most resistant populations also have the lowest fitness costs as measured by growth rate in the ancestral environment. Furthermore, after controlling for differences in the evolutionary dynamics of resistance to different herbicides, we also detect significant positive correlations between resistance, fitness in the ancestral environment and cross-resistance to other herbicides. We attribute this to the highest levels of nontarget-site resistance being achieved by fixing mutations that more broadly affect cellular physiology, which results in both more cross-resistance and less overall antagonistic pleiotropy on maximum growth rate. Consequently, the lack of classical ecological trade-offs could present a major challenge for herbicide resistance management.     

Natural Selection and the Frequency Distributions of ``silent' DNA Polymorphism in Drosophila

In Escherichia coli, Saccharomyces cerevisiae, and Drosophila melanogaster, codon bias may be maintained by a balance among mutation pressure, genetic drift, and natural selection favoring translationally superior codons. Under such an evolutionary model, silent mutations fall into two fitness categories: preferred mutations that increase codon bias and unpreferred changes in the opposite direction. This prediction can be tested by comparing the frequency spectra of synonymous changes segregating within populations; natural selection will elevate the frequencies of advantageous mutations relative to that of deleterious changes. The frequency distributions of preferred and unpreferred mutations differ in the predicted direction among 99 alleles of two D. pseudoobscura genes and five alleles of eight D. simulans genes. This result confirms the existence of fitness classes of silent mutations. Maximum likelihood estimates suggest that selection intensity at silent sites is, on average, very weak in both D. pseudoobscura and D. simulans (|N(e)s| & 1). Inference of evolutionary processes from within-species sequence variation is often hindered by the assumption of a stationary frequency distribution. This assumption can be avoided when identifying the action of selection and tested when estimating selection intensity.     

Bacterial Adaptation through Loss of Function

The metabolic capabilities and regulatory networks of bacteria have been optimized by evolution in response to selective pressures present in each species'' native ecological niche. In a new environment, however, the same bacteria may grow poorly due to regulatory constraints or biochemical deficiencies. Adaptation to such conditions can proceed through the acquisition of new cellular functionality due to gain of function mutations or via modulation of cellular networks. Using selection experiments on transposon-mutagenized libraries of bacteria, we illustrate that even under conditions of extreme nutrient limitation, substantial adaptation can be achieved solely through loss of function mutations, which rewire the metabolism of the cell without gain of enzymatic or sensory function. A systematic analysis of similar experiments under more than 100 conditions reveals that adaptive loss of function mutations exist for many environmental challenges. Drawing on a wealth of examples from published articles, we detail the range of mechanisms through which loss-of-function mutations can generate such beneficial regulatory changes, without the need for rare, specific mutations to fine-tune enzymatic activities or network connections. The high rate at which loss-of-function mutations occur suggests that null mutations play an underappreciated role in the early stages of adaption of bacterial populations to new environments.     

Pleiotropy and GAL pathway degeneration in yeast

Traits that do not contribute to fitness are expected to be lost during the course of evolution, either as a result of selection or drift. The Leloir pathway of galactose metabolism (GAL) is an extensively studied metabolic pathway that degenerated on at least three independent occasions during the evolutionary diversification of yeasts, suggesting that the pathway is costly to maintain in environments that lack galactose. Here I test this hypothesis by competing GAL pathway deletion mutants of Saccharomyces cerevisiae against an isogenic strain with an intact GAL pathway under conditions where expression of the pathway is normally induced, repressed, or uninduced. These experiments do not support the hypothesis that pleiotropy drives GAL pathway degeneration, because mutations that knock out individual GAL genes do not tend to increase fitness in the absence of galactose. At a molecular level, this result can be explained by the fact that yeast uses inexpensive regulatory proteins to tightly regulate the expression of structural genes that are costly to express. I argue that these results have general relevance for our understanding of the fitness consequences of gene disruption in yeast.     

Multi-trait Selection, Adaptation, and Constraints on the Evolution of Burst Swimming Performance

Whole organism performance represents the integration of numerousphysiological, morphological, and behavioral traits. How adaptivechanges in performance evolve therefore requires an understandingof how selection acts on multiple integrated traits. Two approachesthat lend themselves to studying the evolution of performancein natural populations are the use of quantitative geneticsmodels for estimating the strength of selection acting on multiplequantitative traits and ecological genetic comparisons of populationsexhibiting phenotypic differences correlated with environmentalvariation. In both cases, the ultimate goal is to understandhow suites of traits and trade-offs between competing functionsrespond to natural selection. Here we consider how these twocomplimentary approaches can be applied to study the adaptiveevolution of escape performance in fish. We first present anextension of Arnold's (1983) quantitative genetic approach thatexplicitly considers how trade-offs between different componentsof performance interact with the underlying genetics. We proposethat such a model can reveal the conditions under which multipleselection pressures will cause adaptive change in traits thatinfluence more than one component of fitness. We then reviewwork on the Atlantic silversides and Trinidadian guppies astwo case studies where an ecological genetics approach has beensuccessfully applied to evaluate how the evolution of escapeperformance trades-off with other components of fitness. Weconclude with the general lesson that whole organism performanceis embedded in a complex phenotype, and that the net outcomeof selection acting on different aspects of the organism willoften result in a compromise among competing influences.     

The effect of pathogens on selection against deleterious mutations in Drosophila melanogaster

In natural populations, fitness is reduced by both deleterious mutations and parasites. Few studies have examined interactions between these two factors, particularly at the level of individual genes. We examined how the presence of a bacterial pathogen, Pseudomonas aeruginosa, affected the selection against each of eight deleterious mutations in Drosophila melanogaster. We found that mutations tended to become more deleterious in the presence of disease. This increase in the average selection was primarily due to three genes with the remainder showing little evidence of change.     

Importance of genetic recombination for the preservation and progress of species in the course of evolution

The role of genetic recombinations is considered in the context of ecological stability of organisms. The ecological stability is taken as a special notion distinct from fitness in its original sense as the Maltusian parameter according to R. Fisher. The genetic exchange within the species provides the recovery of a species specific level of ecological stability that is lowered in particular individuals as a result of the accumulation of mutations in microevolutionary processes. It is supposed that the accumulation of the mutations that decrease organisms' ecological stability leads to the action of truncated selection. This type of selection explains the advantage of recombination in the model of A.S. Kondrashov (1982). In the evolving species, ecological stability is gradually increasing in the process of evolution as a result of hybridization between the narrow-specialized races. Genetic recombinations provide a constant DNA homogenization within the species and, therefore, the species integrity as an elementary structure responsible for the preservation and rise in the level of ecological stability of organisms in evolving lineages.