Evolution as resistance to entropy. I. Mechanisms of species homeostasis

The idea is discussed that the common output of any evolution is creation of the entities that are increasingly resistant to further evolution. The moving force of evolution is entropy, the tendency to disorder. This general aspiration for chaos is a cause of the mortality of organisms and species, however, being prerequisite for any movement, it creates (by chance) novelties, which may occur (by chance) more resistant to further decay and thus survive. The surviving of those who survive is the most general principle of evolution discovered by Darwin for particular case of biological evolution. The second law of thermodynamics states that our Universe is perishing but its ontology is such that it creates resistance to destruction. The evolution is a history of this resistance. Not only those who die do not survive but also those who evolve. The entities that change (evolve) rapidly disappear rapidly and by this reason they are not observed among both the fossils and now-living organisms. We know only about long-living species. All the existing organisms are endowed with an ability to resist other changing. The following main achievements of the species homeostasis are discussed: high fidelity of DNA replication and effective mechanisms of DNA repair; diploidy; normalizing selection; truncated selection; heterozygote superiority; ability to change phenotype adaptively without changing genotype; parental care and the K-strategy of reproduction; behavior that provides independence of the environment. The global resistance of the living systems to entropy is provided the state that all the essential in biology is determined not by physical-chemical interactions but could semantic rules. A conception of "potential zygotic information" that determines the rules of ontogenesis is proposed. A zygote does not contain this information in explicit form. It is created de novo step by step during ontogenesis and it could not be decoded beforehand. The experimental data on the adaptive mutagenesis and the relevant hypothesis are discussed. It is concluded that the special mechanisms for speeding-up of evolution as created by evolution are impossible conceptually.     

Biological species is the only possible form of existence for higher organisms: the evolutionary meaning of sexual reproduction

   

Consistent holistic view of sexual species as the highest form of biological existence is presented. The Weismann's idea that sex and recombination provide the variation for the natural selection to act upon is dominated in most discussions of the biological meaning of the sexual reproduction. Here, the idea is substantiated that the main advantage of sex is the opposite: the ability to counteract not only extinction but further evolution as well. Living systems live long owing to their ability to reproduce themselves with a high fidelity. Simple organisms (like bacteria) reach the continued existence due to the high fidelity of individual genome replication. In organisms with a large genome and complex development, the achievable fidelity of DNA replication is not enough for the precise reproduction of the genome. Such species must be capable of surviving and must remain unchanged in spite of the continuous changes of their genes. This problem has no solution in the frame of asexual ("homeogenomic") lineages. They would rapidly degrade and become extinct or blurred out in the course of the reckless evolution. The core outcome of the transition to sexual reproduction was the creation of multiorganismic entity - biological species. Individual organisms forfeited their ability to reproduce autonomously. It implies that individual organisms forfeited their ability to substantive evolution. They evolve as a part of the biological species. In case of obligatory sexuality, there is no such a thing as synchronic multi-level selection. Natural selection cannot select anything that is not a unit of reproduction. Hierarchy in biology implies the functional predestination of the parts for the sake of the whole. A crucial feature of the sexual reproduction is the formation of genomes of individual organisms by random picking them over from the continuously shuffled gene pool instead of the direct replication of the ancestor's genome. A clear anti-evolutionary consequence of the sexuality is evident from the fact that the genotypes of the individuals with an enhanced competitiveness are not transmitted to the next generation. Instead, after mating with "ordinary" individuals, these genotypes scatter and rearrange in new gene combinations, thus preventing the winner from exploiting the success.     

Promotion of evolution by intracellular coexistence of mutator and normal DNA polymerases

The efficient evolution of a population requires both genetic diversity and stable reproduction of advantageous genotypes. The accuracy of DNA replication guarantees the stable reproduction, while errors during DNA replication produce the genetic diversity. Thus, one key to the promotion of evolution is inherent in DNA replication. In bacteria, replication forks progress bidirectionally from the single origin of replication on a genome. One replication fork contains two DNA polymerase molecules so that four DNA polymerases simultaneously carry out the replication of a genome. It is generally believed that the fidelity of the intracellular DNA polymerases is identical (parity strategy). To test this, we examined the effects of the intracellular coexistence of a mutator polymerase with low fidelity and a normal polymerase with high fidelity on adaptive evolution (disparity strategy). From the analysis using genetic algorithms based on the bacterial replication, it was found that the population using the disparity strategy could further expand its genetic diversity and preserve the advantageous genotypes more profoundly than the parity population. This strongly suggests that bacteria replicating with a disparity strategy may undergo rapid evolution, particularly during severe environmental changes. The implications of the conspicuous adaptability of Escherichia coli mutator strains are discussed in this context.     

Thermodynamic perspectives on genetic instructions, the laws of biology and diseased states

This article examines in a broad perspective entropy and some examples of its relationship to evolution, genetic instructions and how we view diseases. Living organisms are programmed by functional genetic instructions (FGI), through cellular communication pathways, to grow and reproduce by maintaining a variety of hemistable, ordered structures (low entropy). Living organisms are far from equilibrium with their surrounding environmental systems, which tends towards increasing disorder (increasing entropy). Organisms free themselves from high entropy (high disorder) to maintain their cellular structures for a period of time sufficient to allow reproduction and the resultant offspring to reach reproductive ages. This time interval varies for different species. Bacteria, for example need no sexual parents; dividing cells are nearly identical to the previous generation of cells, and can begin a new cell cycle without delay under appropriate conditions. By contrast, human infants require years of care before they can reproduce. Living organisms maintain order in spite of their changing surrounding environment that decreases order according to the second law of thermodynamics. These events actually work together since living organisms create ordered biological structures by increasing local entropy. From a disease perspective, viruses and other disease agents interrupt the normal functioning of cells. The pressure for survival may result in mechanisms that allow organisms to resist attacks by viruses, other pathogens, destructive chemicals and physical agents such as radiation. However, when the attack is successful, the organism can be damaged until the cell, tissue, organ or entire organism is no longer functional and entropy increases.     

A General Method for Modeling Population Dynamics and Its Applications

Studying populations, be it a microbe colony or mankind, is important for understanding how complex systems evolve and exist. Such knowledge also often provides insights into evolution, history and different aspects of human life. By and large, populations’ prosperity and decline is about transformation of certain resources into quantity and other characteristics of populations through growth, replication, expansion and acquisition of resources. We introduce a general model of population change, applicable to different types of populations, which interconnects numerous factors influencing population dynamics, such as nutrient influx and nutrient consumption, reproduction period, reproduction rate, etc. It is also possible to take into account specific growth features of individual organisms. We considered two recently discovered distinct growth scenarios: first, when organisms do not change their grown mass regardless of nutrients availability, and the second when organisms can reduce their grown mass by several times in a nutritionally poor environment. We found that nutrient supply and reproduction period are two major factors influencing the shape of population growth curves. There is also a difference in population dynamics between these two groups. Organisms belonging to the second group are significantly more adaptive to reduction of nutrients and far more resistant to extinction. Also, such organisms have substantially more frequent and lesser in amplitude fluctuations of population quantity for the same periodic nutrient supply (compared to the first group). Proposed model allows adequately describing virtually any possible growth scenario, including complex ones with periodic and irregular nutrient supply and other changing parameters, which present approaches cannot do.     

A quasispecies approach to the evolution of sexual replication in unicellular organisms

This study develops a simplified model describing the evolutionary dynamics of a population composed of obligate sexually and asexually reproducing, unicellular organisms. The model assumes that the organisms have diploid genomes consisting of two chromosomes, and that the sexual organisms replicate by first dividing into haploid intermediates, which then combine with other haploids, followed by the normal mitotic division of the resulting diploid into two new daughter cells. We assume that the fitness landscape of the diploids is analogous to the single-fitness-peak approach often used in single-chromosome studies. That is, we assume a master chromosome that becomes defective with just one point mutation. The diploid fitness then depends on whether the genome has zero, one, or two copies of the master chromosome. We also assume that only pairs of haploids with a master chromosome are capable of combining so as to produce sexual diploid cells, and that this process is described by second-order kinetics. We find that, in a range of intermediate values of the replication fidelity, sexually reproducing cells can outcompete asexual ones, provided the initial abundance of sexual cells is above some threshold value. The range of values where sexual reproduction outcompetes asexual reproduction increases with decreasing replication rate and increasing population density. We critically evaluate a common approach, based on a group selection perspective, used to study the competition between populations and show its flaws in addressing the evolution of sex problem.     

Gene copy number variations as signatures of adaptive evolution in the parthenogenetic,plant‐parasitic nematode Meloidogyne incognita

Adaptation to changing environmental conditions represents a challenge to parthenogenetic organisms, and until now, how phenotypic variants are generated in clones in response to the selection pressure of their environment remains poorly known. The obligatory parthenogenetic root‐knot nematode species Meloidogyne incognita has a worldwide distribution and is the most devastating plant‐parasitic nematode. Despite its asexual reproduction, this species exhibits an unexpected capacity of adaptation to environmental constraints, for example, resistant hosts. Here, we used a genomewide comparative hybridization strategy to evaluate variations in gene copy numbers between genotypes of M. incognita resulting from two parallel experimental evolution assays on a susceptible vs. resistant host plant. We detected gene copy number variations (CNVs) associated with the ability of the nematodes to overcome resistance of the host plant, and this genetic variation may reflect an adaptive response to host resistance in this parthenogenetic species. The CNV distribution throughout the nematode genome is not random and suggests the occurrence of genomic regions more prone to undergo duplications and losses in response to the selection pressure of the host resistance. Furthermore, our analysis revealed an outstanding level of gene loss events in nematode genotypes that have overcome the resistance. Overall, our results support the view that gene loss could be a common class of adaptive genetic mechanism in response to a challenging new biotic environment in clonal animals.     

Antibiotic resistant pathogen outbreak investigation: an interdisciplinary module to teach fundamentals of evolutionary biology

The evolution of resistance to antibiotics provides a timely and relevant topic for teaching undergraduate students evolutionary biology. Here, we present a module incorporating modified sequencing data from eight antibiotic resistant pathogen outbreaks in hospital settings with bioinformatics and phylogenetic analyses. This module uses whole genome sequencing data from hospital outbreaks investigated by the Centers for Disease Control and Prevention to provide examples of antibiotic resistance spread. Students work in groups to analyze outbreak data to identify the bacterial species and antibiotic resistance genes, to infer a phylogenetic tree examining relatedness among isolates, and to determine a possible source of the outbreak. Students then compile their results in individual reports and provide recommendations for preventing the further spread of antibiotic resistant organisms. In addition to providing genomic outbreak data, we include a teaching concepts guide discussing three integral components of the module: how evolutionary biology concepts of natural selection and competition impact antibiotic resistance; outbreak investigation information to aid in phylogenetic analysis and creation of recommendations; and instructions for the bioinformatics protocol. Completion of this module provides students an opportunity to think critically about the evolution of resistance, practice bioinformatics techniques, and relate evolutionary biology to current events.     

Origin and evolution of life and intellect from the point of view of information processing]

Beginning of life and intellect on the Earth is determined by the fact that synthesis of semantic information about algorithms of chemical transformation for appointed classes of chemical compounds is not accompanied by the information synthesis, but is controlled by chance in genetic material. Genetic information as memorizing accidental choice always arises as a result of the environment interaction, when memorizing realization in the form of repeated reproduction occurs on the basis of processes radically different from those which created initial genetic chance. Such stepped synthesis of information has hierarchical character and it is described by entropy of different dimensions. Entropy is determined by conditional probabilities. Therefore as a form of life becomes complicated, the entropy is decreased within the limits of the given hierarchical step. The part of entropy depending on the number of elements of the system (cells, individuals, etc.) always increases in the memorizing process, i. e. life defines the maximum of entropy production (but not the minimum like in nature). This fact settles paradoxes of chance in Darwinism: as a result of entropy decrease within higher hierarchical step the simbiotic processes for more complex forms of life can arise with great probability. For instance, rapidity of evolution of human brain given by supplementary chance in the mechanism of fecundation under the conditions of biochemical pressure of androgenes both, on the brain development and on muscular force at the same time. Synthesis of information in the brain is determined by the same principles, but extremums of the thermo-dynamic potential (their analogues in logic) are based on an arbitrary system of axioms. As a whole life and intellect are not fluctuations pointed against entropy increases, but they arose according to spontaneous process of entropy development.     

Elimination of altered karyotypes by sexual reproduction preserves species identity.

Resolving the persistence of sexual reproduction despite its overwhelming costs (known as the paradox of sex) is one of the most persistent challenges of evolutionary biology. In thinking about this paradox, the focus has traditionally been on the evolutionary benefits of genetic recombination in generating offspring diversity and purging deleterious mutations. The similarity of pattern between evolution of organisms and evolution among cancer cells suggests that the asexual process generates more diverse genomes owing to less controlled reproduction systems, while sexual reproduction generates more stable genomes because the sexual process can serve as a mechanism to "filter out" aberrations at the chromosome level. Our reinterpretation of data from the literature strongly supports this hypothesis. Thus, the principal consequence of sexual reproduction is the reduction of drastic genetic diversity at the genome or chromosome level, resulting in the preservation of species identity rather than the provision of evolutionary diversity for future environmental challenges. Genetic recombination does contribute to genetic diversity, but it does so secondarily and within the framework of the chromosomally defined genome.     

Evolutionary computation

Evolution does not require DNA, or even living organisms. In computer science, the field known as 'evolutionary computation' uses evolution as an algorithmic tool, implementing random variation, reproduction and selection by altering and moving data within a computer. This harnesses the power of evolution as an alternative to the more traditional ways to design software or hardware. Research into evolutionary computation should be of interest to geneticists, as evolved programs often reveal properties - such as robustness and non-expressed DNA - that are analogous to many biological phenomena.     

Steering Evolution with Sequential Therapy to Prevent the Emergence of Bacterial Antibiotic Resistance

The increasing rate of antibiotic resistance and slowing discovery of novel antibiotic treatments presents a growing threat to public health. Here, we consider a simple model of evolution in asexually reproducing populations which considers adaptation as a biased random walk on a fitness landscape. This model associates the global properties of the fitness landscape with the algebraic properties of a Markov chain transition matrix and allows us to derive general results on the non-commutativity and irreversibility of natural selection as well as antibiotic cycling strategies. Using this formalism, we analyze 15 empirical fitness landscapes of E. coli under selection by different β-lactam antibiotics and demonstrate that the emergence of resistance to a given antibiotic can be either hindered or promoted by different sequences of drug application. Specifically, we demonstrate that the majority, approximately 70%, of sequential drug treatments with 2–4 drugs promote resistance to the final antibiotic. Further, we derive optimal drug application sequences with which we can probabilistically ‘steer’ the population through genotype space to avoid the emergence of resistance. This suggests a new strategy in the war against antibiotic–resistant organisms: drug sequencing to shepherd evolution through genotype space to states from which resistance cannot emerge and by which to maximize the chance of successful therapy.     

Viral RNA and evolved mutational robustness.

Many properties of organisms show great robustness against mutations. Whether this robustness is an evolved property or intrinsic to genetic systems is by and large unknown. An evolutionary origin of robustness would require a rethinking of key concepts in the field of molecular evolution, such as gene-specific neutral mutation rates, or the context-independence of deleterious mutations. We provide evidence that mutational robustness of the genome of RNA viruses to mutational changes in secondary structure has evolved. J. Exp. Zool. ( Mol. Dev. Evol.) 285:119-127, 1999.     

Evolution of herbicide resistance in weeds: vertically transmitted fungal endophytes as genetic entities

The appearance of heritable resistance to herbicides in weeds is an evolutionary process driven by human selection. Assuming that spontaneous and random mutations originate herbicide resistance genes, which are selected by selection pressure imposed by herbicides, is the simplest model to understand how this phenomenon appears and increases in weed populations. However, the rate of herbicide resistance evolution is not only determined by the amount of genetic variation within the populations and the selection pressure exerted by herbicides, but also by factors related to genetics, biology and ecology of weeds. The inheritance of the resistance genes, the mating patterns of the populations, the relative fitness of susceptible and resistant phenotypes and gene flow processes also control the mentioned rate. Many cool season grasses are often infected by fungal symbiotic endophytes (Neotyphodium spp.). These organisms modify the physiology, ecology and reproductive biology of their hosts, conferring greater tolerance to biotic and abiotic stresses, greater competitive ability and the capacity of reducing ecosystem biodiversity. In this work, we present new empirical data and propose new theoretical support on how these microbial symbionts can modulate the evolution of herbicide resistance in weeds. Fungal endophytes are vertically transmitted, and may act as genetic entities altering the evolution of herbicide resistance by reducing herbicide efficacy (delaying effect on evolution). In addition, indirect evidence suggests that fungal endophytes might reduce the fitness penalty associated with the newly arisen resistant phenotypes. The importance and dynamic of these opposite effects is discussed.     

Increased resistance to generalist herbivores in invasive populations of the California poppy (Eschscholzia californica)

Escape from enemies in the native range is often assumed to contribute to the successful invasion of exotic species. Following optimal defence theory, which assumes a trade‐off between herbivore resistance and plant growth, some have predicted that the success of invasive species could be the result of the evolution of lower resistance to herbivores and increased allocation of resources to growth and reproduction. Lack of evidence for ubiquitous costs of producing plant toxins, and the recognition that invasive species may escape specialist, but not generalist enemies, has led to a new prediction: invasive species may escape ecological trade‐offs associated with specialist herbivores, and evolve increased, rather than decreased, production of defensive compounds that are effective at deterring generalist herbivores in the introduced range. We tested the performance of two generalist lepidopteran herbivores, Trichoplusia ni and Orgyia vetusta, when raised on diets of native and invasive populations of the California poppy, Eschscholzia californica. Pupae of T. ni were significantly larger when reared on native populations. Similarly, caterpillars of O. vetusta performed significantly better when raised on native populations, indicating that invasive populations of the California poppy are more resistant to herbivores than native populations. The chance of successful establishment of some non‐indigenous plant species may be increased by retaining resistance to generalist herbivores, and in some cases, invasive species may be able to escape ecological trade‐offs in their new range and evolve, as we observed, even greater resistance to generalist herbivores than native plants.     

Adaptive molecular evolution of HINTW,a female-specific gene in birds

It is well established that many genes on the male-specific Y chromosome of organisms such as mammals are involved in male reproduction and may evolve rapidly because of positive selection on male reproductive traits. In contrast, very little is known about the function and evolution of W-linked genes restricted to the female genome of organisms with female heterogamety. For birds (males ZZ, females ZW), only one W-linked gene (HINTW) is sufficiently different from its Z-linked homolog to indicate a female-specific function. Here, we report that HINTW shows evidence of adaptive molecular evolution, implying strong positive selection for new functional properties in female birds. Moreover, because HINTW is expressed in the gonads of female birds just before sexual differentiation and is thus a candidate for sex determination, it suggests adaptive evolution related to female development. This provides the first example of Darwinian evolution of a gene restricted to the female genome of any organism. Given that HINTW exists in multiple copies on W, similar to some testis-specific genes amplified on mammalian Y, avian HINTW may thus potentially represent a female parallel to the organization and evolution of Y chromosome genes involved in male reproduction and development.     

Thermodynamic stability of ecosystems

The stability of ecosystems during periods of stasis in their macro-evolutionary trajectory is studied from a non-equilibrium thermodynamic perspective. Individuals of the species are considered as units of entropy production and entropy exchange in an open thermodynamic system. Within the framework of the classical theory of irreversible thermodynamics, and under the condition of constant external constraints, such a system will naturally evolve toward a globally stable thermodynamic stationary state. It is thus suggested that the ecological steady state, or stasis, is a particular case of the thermodynamic stationary state, and that the evolution of community stability through natural selection is a manifestation of non-equilibrium thermodynamic directives. Furthermore, it is argued that punctuation of stasis leading to ecosystem succession, may be a manifestation of non-equilibrium "phase transitions" brought on by a change of external constraints through a thermodynamic critical point.