Fitness Of Genotypes Research Articles

Universality Classes of Interaction Structures for NK Fitness Landscapes

Kauffman's NK-model is a paradigmatic example of a class of stochastic models of genotypic fitness landscapes that aim to capture generic features of epistatic interactions in multilocus systems. Genotypes are represented as sequences of $L$ binary loci. The fitness assigned to a genotype is a sum of contributions, each of which is a random function defined on a subset of $k \le L$ loci. These subsets or neighborhoods determine the genetic interactions of the model. Whereas earlier work on the NK model suggested that most of its properties are robust with regard to the choice of neighborhoods, recent work has revealed an important and sometimes counter-intuitive influence of the interaction structure on the properties of NK fitness landscapes. Here we review these developments and present new results concerning the number of local fitness maxima and the statistics of selectively accessible (that is, fitness-monotonic) mutational pathways. In particular, we develop a unified framework for computing the exponential growth rate of the expected number of local fitness maxima as a function of $L$, and identify two different universality classes of interaction structures that display different asymptotics of this quantity for large $k$. Moreover, we show that the probability that the fitness landscape can be traversed along an accessible path decreases exponentially in $L$ for a large class of interaction structures that we characterize as locally bounded. Finally, we discuss the impact of the NK interaction structures on the dynamics of evolution using adaptive walk models.

Use and misuse of temperature normalisation in meta-analyses of thermal responses of biological traits.

There is currently unprecedented interest in quantifying variation in thermal physiology among organisms, especially in order to understand and predict the biological impacts of climate change. A key parameter in this quantification of thermal physiology is the performance or value of a rate, across individuals or species, at a common temperature (temperature normalisation). An increasingly popular model for fitting thermal performance curves to data—the Sharpe-Schoolfield equation—can yield strongly inflated estimates of temperature-normalised rate values. These deviations occur whenever a key thermodynamic assumption of the model is violated, i.e., when the enzyme governing the performance of the rate is not fully functional at the chosen reference temperature. Using data on 1,758 thermal performance curves across a wide range of species, we identify the conditions that exacerbate this inflation. We then demonstrate that these biases can compromise tests to detect metabolic cold adaptation, which requires comparison of fitness or rate performance of different species or genotypes at some fixed low temperature. Finally, we suggest alternative methods for obtaining unbiased estimates of temperature-normalised rate values for meta-analyses of thermal performance across species in climate change impact studies.

The advantage of recombination when selection is acting at many genetic Loci

Natural selection can act at many loci across the genome. But as the number of polymorphic loci increases linearly, the number of possible genotypic combinations increases exponentially. Consequently, a finite population – even a very large population – contains only a small sample of all possible multi-locus genotypes. In this paper, we revisit the classic Fisher-Muller models of recombination, taking into account the abundant standing variation that is commonly seen in natural populations. We show that the generation of new genotypic combinations through recombination is an important component of adaptive evolution based on multi-locus selection. Specifically, high-fitness genotypes are expected to be absent from the initial population when the frequencies of favorable alleles at the selected loci are low. But as the allele frequencies rise in response to selection the missing genotypes will be generated by recombination. Given recombination, if the average frequency of the favored alleles at the various selected loci is equal to p, then the expected number of favorable alleles per chromosome will be equal to pL, where L is the number of loci. As the value of p approaches unity at the selected loci, the number of favorable alleles per chromosome will approach a value of L, i.e., at the end of the selection process a favorable allele will be found at all loci. In the absence of recombination, however, selection will be limited to the highest-fitness genotypes that are already present in the initial population. We point out that the fitness of such initial genotypes is far less than the theoretical maximum fitness because they contain a favorable allele at only a fraction of the loci. Consequently, recombination acts to unblock the adaptive response to multi-locus selection in finite populations. Using simulations, we show that the sexual population can withstand invasion by newly-arising asexual clones. These results help explain the maintenance of sexual reproduction in natural populations.

Fitness consequences of occasional outcrossing in a functionally asexual plant (Oenothera biennis).

Many clonal organisms occasionally outcross, but the long-term consequences of such infrequent events are often unknown. During fiveyears, representing three to five plant generations, we followed 16 experimental field populations of the forb, Oenothera biennis, originally planted with the same 18 original genotypes. Oenothera biennis usually self fertilizes, which, due to its genetic system (permanent translocation heterozygosity), results in seeds that are clones of the maternal plant. However, rare outcrossing produces genetically novel offspring (but without recombination or increased heterozygosity). We sought to understand whether novel genotypes produced through natural outcrossing had greater fecundity or different multigenerational dynamics compared to our original genotypes. We further assessed whether any differences in fitness or abundances through time between original and novel genotypes were exaggerated in the presence vs. absence of insect herbivores. Over the course of the experiment, we genotyped >12,500 plants using microsatellite DNA markers to identify and track the frequency of specific genotypes and estimated fecundity on a subset (>3,000) of plants. The effective outcrossing rate was 7.3% in the first year and ultimately 50% of the plants were of outcrossed origin by the final year of the experiment. Lifetime fruit production per plant was on average 32% higher across all novel genotypes produced via outcrossing compared to the original genotypes, and this fecundity advantage was significantly enhanced in populations lacking herbivores. Among 43 novel genotypes that were abundant enough to phenotype with replication, plants produced nearly 30% more fruits than the average of their specific two parental genotypes, and marginally more fruits (8%) than their most fecund parent. Mean per capita fecundity of novel genotypes predicted their relative frequencies at the end of the experiment. Novel genotypes increased more dramatically in herbivore-present compared to suppressed populations (45% vs. 27% of all plants), countering the increased competition from dandelions (Taraxacum officinale) that resulted from herbivore suppression. Increased interspecific competition likely also lead to the lower realized fitness of novel vs. original genotypes in herbivore-suppressed populations. These results demonstrate that rare outcrossing and the generation of novel genotypes can create high-fecundity progeny, with the biotic environment influencing the dynamical outcome of such advantages.

Genome-Wide Screen for Saccharomyces cerevisiae Genes Contributing to Opportunistic Pathogenicity in an Invertebrate Model Host.

Environmental opportunistic pathogens can exploit vulnerable hosts through expression of traits selected for in their natural environments. Pathogenicity is itself a complicated trait underpinned by multiple complex traits, such as thermotolerance, morphology, and stress response. The baker’s yeast, Saccharomyces cerevisiae, is a species with broad environmental tolerance that has been increasingly reported as an opportunistic pathogen of humans. Here we leveraged the genetic resources available in yeast and a model insect species, the greater waxmoth Galleria mellonella, to provide a genome-wide analysis of pathogenicity factors. Using serial passaging experiments of genetically marked wild-type strains, a hybrid strain was identified as the most fit genotype across all replicates. To dissect the genetic basis for pathogenicity in the hybrid isolate, bulk segregant analysis was performed which revealed eight quantitative trait loci significantly differing between the two bulks with alleles from both parents contributing to pathogenicity. A second passaging experiment with a library of deletion mutants for most yeast genes identified a large number of mutations whose relative fitness differed in vivo vs. in vitro, including mutations in genes controlling cell wall integrity, mitochondrial function, and tyrosine metabolism. Yeast is presumably subjected to a massive assault by the innate insect immune system that leads to melanization of the host and to a large bottleneck in yeast population size. Our data support that resistance to the innate immune response of the insect is key to survival in the host and identifies shared genetic mechanisms between S. cerevisiae and other opportunistic fungal pathogens.

Phenotypic Stability of Zea mays Grain Yield and Its Attributing Traits under Drought Stress.

Phenotypic stability under stress environment facilitate the fitness of genotype and opens new horizons to explore the cryptic genetic variation. Variation in tolerance to drought stress, a major grain yield constraint to global maize production, was identified, at the phenotypic and genotypic level. Here we found a prominent hybrid H9 that showed fitness over four growing seasons for grain yield under water stress conditions. Genotypic and phenotypic correlation of yield attributing traits over four seasons demonstrated that cobs per plant, 100 seed weight, number of grains rows per cob, total dry matter, cob diameter had positive association (r2 = 0.3–0.9) to grain yield. The perturbation was found for chlorophyll content as it showed moderate to strong association (P < 0.01) over four seasons, might be due to environment or genotype dependent. Highest heritability (95%) and genetic advance (79%) for grain yield was found in H9 over four consecutive crop growing seasons. Combined analysis over four seasons showed that studied variables together explained 85% of total variation in dependent structure (grain yield) obtained by Principal component analysis. This significant finding is the best example of phenotypic stability of grain yield in H9 and made it best fitted for grain yield under drought stress scenario. Detailed genetic analysis of H9 will help us to identify significant loci and alleles that made H9 the best fitted and it could serve as a potential source to generate novel transgressive levels of tolerance for drought stress in arid/semiarid regions.

The Model of Fitness in a Heterogeneous Environment on Reaction Norms

Abstract The understanding of genetic mechanisms of natural selection to a large extent became possible as a result of modelling research carried out in the fields of evolutionary and population genetics. However, genetic models cannot be considered exhaustive in the description of natural selection because a phenotype of individual, environment and fitness remains beyond their framework. Consequently, the value of fitness is not derived from the algorithmic model but arbitrarily assigned by a researcher to genotypes in their genetic formula. This work proposes a model of genotype fitness in heterogeneous environments on reaction norms in connection with the genetic structure of the population. Two equations represent the model. The first is an incomplete second order polynomial that describes the dependence of fitness on the phenotype of an adaptive trait and environmental conditions. The second is a linear equation of the reaction norm of the adaptive trait that determines its phenotype in specific environmental conditions. According to the model algorithms, rating of fitness in the population, and, consequently, their probability of selection, is determined by phenotype optimality and their norm of reaction in certain environmental conditions.

Haploid selection within a single ejaculate increases offspring fitness

An inescapable consequence of sex in eukaryotes is the evolution of a biphasic life cycle with alternating diploid and haploid phases. The occurrence of selection during the haploid phase can have far-reaching consequences for fundamental evolutionary processes including the rate of adaptation, the extent of inbreeding depression, and the load of deleterious mutations, as well as for applied research into fertilization technology. Although haploid selection is well established in plants, current dogma assumes that in animals, intact fertile sperm within a single ejaculate are equivalent at siring viable offspring. Using the zebrafish Danio rerio, we show that selection on phenotypic variation among intact fertile sperm within an ejaculate affects offspring fitness. Longer-lived sperm sired embryos with increased survival and a reduced number of apoptotic cells, and adult male offspring exhibited higher fitness. The effect on embryo viability was carried over into the second generation without further selection and was equally strong in both sexes. Sperm pools selected by motile phenotypes differed genetically at numerous sites throughout the genome. Our findings clearly link within-ejaculate variation in sperm phenotype to offspring fitness and sperm genotype in a vertebrate and have major implications for adaptive evolution.

Cause or consequence? Exploring the role of phenotypic plasticity and genetic polymorphism in the emergence of phenotypic spatial patterns of the European eel

The European eel (Anguilla anguilla), and generally, temperate eels, are relevant species for studying adaptive mechanisms to environmental variability because of their large distribution areas and their limited capacity of local adaptation. In this context, GenEveel, an individual-based optimization model, was developed to explore the role of adaptive phenotypic plasticity and genetic-dependent habitat selection, in the emergence of observed spatial life-history traits patterns for eels. Results suggest that an interaction of genetically and environmentally controlled growth may be the basis for genotype-dependent habitat selection, whereas plasticity plays a role in changes in life-history traits and demographic attributes. Therefore, this suggests that those mechanisms are responses to address environmental heterogeneity. Moreover, this brings new elements to explain the different life strategies of males and females. A sensitivity analysis showed that the parameters associated with the optimization of fitness and growth genotype were crucial in reproducing the spatial life-history patterns. Finally, it raises the question of the impact of anthropogenic pressures that can cause direct mortalities but also modify demographic traits and act as a selection pressure.

With a little help from my friends: cooperation can accelerate the rate of adaptive valley crossing

BackgroundNatural selection favors changes that lead to genotypes possessing high fitness. A conflict arises when several mutations are required for adaptation, but each mutation is separately deleterious. The process of a population evolving from a genotype encoding for a local fitness maximum to a higher fitness genotype is termed an adaptive peak shift.ResultsHere we suggest cooperative behavior as a factor that can facilitate adaptive peak shifts. We model cooperation in a public goods scenario, wherein each individual contributes resources that are later equally redistributed among all cooperating individuals. We use mathematical modeling and stochastic simulations to study the effect of cooperation on peak shifts in both panmictic and structured populations. Our results show that cooperation can substantially affect the rate of complex adaptation. Furthermore, we show that cooperation increases the population diversity throughout the peak shift process, thus increasing the robustness of the population to sudden environmental changes.ConclusionsWe provide a new explanation to adaptive valley crossing in natural populations and suggest that the long term evolution of a species depends on its social behavior.

Sex initiates adaptive evolution by recombination between beneficial loci.

Current theory proposes that sex can increase genetic variation and produce high fitness genotypes if genetic associations between alleles at different loci are non-random. In case beneficial and deleterious alleles at different loci are in linkage disequilibrium, sex may i) recombine beneficial alleles of different loci, ii) liberate beneficial alleles from genetic backgrounds of low fitness, or iii) recombine deleterious mutations for more effective elimination. In our study, we found that the first mechanism dominated the initial phase of adaptive evolution in Brachionus calyciflorus rotifers during a natural selection experiment. We used populations that had been locally adapted to two environments previously, creating a linkage disequilibrium between beneficial and deleterious alleles at different loci in a combined environment. We observed the highest fitness increase when several beneficial alleles of different loci could be recombined, while the other mechanisms were ineffective. Our study thus provides evidence for the hypothesis that sex can speed up adaptation by recombination between beneficial alleles of different loci, in particular during early stages of adaptive evolution in our system. We also suggest that the benefits of sex might change over time and state of adaptive progress.

Genotypic Complexity of Fisher’s Geometric Model

Fisher's geometric model was originally introduced to argue that complex adaptations must occur in small steps because of pleiotropic constraints. When supplemented with the assumption of additivity of mutational effects on phenotypic traits, it provides a simple mechanism for the emergence of genotypic epistasis from the nonlinear mapping of phenotypes to fitness. Of particular interest is the occurrence of reciprocal sign epistasis, which is a necessary condition for multipeaked genotypic fitness landscapes. Here we compute the probability that a pair of randomly chosen mutations interacts sign epistatically, which is found to decrease with increasing phenotypic dimension n, and varies nonmonotonically with the distance from the phenotypic optimum. We then derive expressions for the mean number of fitness maxima in genotypic landscapes comprised of all combinations of L random mutations. This number increases exponentially with L, and the corresponding growth rate is used as a measure of the complexity of the landscape. The dependence of the complexity on the model parameters is found to be surprisingly rich, and three distinct phases characterized by different landscape structures are identified. Our analysis shows that the phenotypic dimension, which is often referred to as phenotypic complexity, does not generally correlate with the complexity of fitness landscapes and that even organisms with a single phenotypic trait can have complex landscapes. Our results further inform the interpretation of experiments where the parameters of Fisher's model have been inferred from data, and help to elucidate which features of empirical fitness landscapes can be described by this model.

Mathematical modelling for variations of inbreeding populations fitness with single and polygenic traits

BackgroundInbreeding mating has been widely accepted as the key mechanism to enhance homozygosity which normally will decrease the fitness of the population. Although this result has been validated by a large amount of biological data from the natural populations, a mathematical proof of these experimental discoveries is still not complete. A related question is whether we can extend the well-established result regarding the mean fitness from a randomly mating population to inbreeding populations. A confirmative answer may provide insights into the frequent occurrence of self-fertilization populations.ResultsThis work presents a theoretic proof of the result that, for a large inbreeding population with directional relative genotype fitness, the mean fitness of population increases monotonically. However, it cannot be extended to the case with over-dominant genotype fitness. In addition, by employing multiplicative intersection hypothesis, we prove that inbreeding mating does decrease the mean fitness of polygenic population in general, but does not decrease the mean fitness with mixed dominant-recessive genotypes. We also prove a novel result that inbreeding depression depends on not only the mating pattern but also genetic structure of population.ConclusionsFor natural inbreeding populations without serious inbreeding depression, our theoretical analysis suggests the majority of its genotypes should be additive or dominant-recessive genotypes. This result gives a reason to explain why many hermaphroditism populations do not show severe inbreeding depression. In addition, the calculated purging rate shows that inbreeding mating purges the deleterious mutants more efficiently than randomly mating does.

Diminishing-returns epistasis decreases adaptability along an evolutionary trajectory.

Populations evolving in constant environments exhibit declining adaptability. Understanding the basis of this pattern could reveal underlying processes determining the repeatability of evolutionary outcomes. In principle, declining adaptability can be due to a decrease in the effect size of beneficial mutations, a decrease in the rate at which they occur, or some combination of both. By evolving Escherichia coli populations started from different steps along a single evolutionary trajectory, we show that declining adaptability is best explained by a decrease in the size of available beneficial mutations. This pattern reflected the dominant influence of negative genetic interactions that caused new beneficial mutations to confer smaller benefits in fitter genotypes. Genome sequencing revealed that starting genotypes that were more similar to one another did not exhibit greater similarity in terms of new beneficial mutations, supporting the view that epistasis acts globally, having a greater influence on the effect than on the identity of available mutations along an adaptive trajectory. Our findings provide support for a general mechanism that leads to predictable phenotypic evolutionary trajectories.

Association between gene polymorphisms and obesity and physical fitness in Korean children.

Obesity is affected by genetic factors and environmental influences. This research was undertaken to identify single nucleotide polymorphisms (SNPs) related to obesity and physical fitness and then to analyse and compare interactions between physical fitness and obesity-associated genotypes. To investigate relationships between physical fitness and major SNPs previously reported to be related to obesity, 68 SNPs in 32 genes were genotyped in 71 Korean children. Tests were conducted to evaluate five elements of physical fitness (speed, aerobic endurance, muscular endurance, muscular strength, and flexibility). The results obtained showed significant (P<0.02) differences in physical fitness scores for the following genotypes: CNR1 (rs1049353; GG), LEP (rs7799039; AA+AG), HHEX (rs1111875; TT), GC (rs16847015; TG+GG), LRP5 (rs4988300; GG+GT), NPY2R (rs2880415; CT+CC), PPY (rs231472; GG), UCP2 (rs660339; CT+TT), CDKN2B (rs10811661; AA+AG), and ADIPOQ (rs266729; CG+GG). Ten physical fitness-related genotypes were newly identified during the present study. This study suggests that classification of genotypes by physical fitness level could be used as an index for predicting the risk of obesity and for selecting individuals for intervention programmes. Furthermore, the study shows that even children participating in the same physical fitness improvement programme can exhibit different genotype dependencies.

Porcine circovirus type 2 (PCV2) evolution before and after the vaccination introduction: A large scale epidemiological study.

Since their commercialization, vaccines against Porcine circovirus type 2 (PCV2) have been the cornerstone control strategy. Nevertheless, the periodic emergence of new genotype waves and the recent reports of vaccine failure outbreaks have raised the question if widespread vaccination strategies could have driven viral evolution and affected different genotype fitness. To investigate this issue an in-deep analysis, based on a bioinformatics and biostatistics approach, has been implemented. ORF2 sequences from vaccinated and non-vaccinated populations (i.e. domestic pigs before and after vaccine introduction and wild boars) were considered. The action of selective forces on PCV2 strains has been analyzed and compared among groups. Remarkable differences were found in the selective forces acting on viral populations circulating in different “immune environments”. Particularly for PCV2a, a directional selection promoting a change in the viral capsid away from the vaccine specific antigenic determinants has been detected after vaccine introduction. Involved amino acids were previously reported to be part of viral epitopes whose variability is responsible of immune escape. Our findings support a change in PCV2 evolutionary pattern after widespread vaccination introduction and stress once more the compulsoriness of a continuous monitoring of PCV2 epidemiology to promptly act in response to the emergence of possible vaccine-escaping mutants.

Predicting patterns of long-term adaptation and extinction with population genetics.

Population genetics struggles to model extinction; standard models track the relative rather than absolute fitness of genotypes, while the exceptions describe only the short-term transition from imminent doom to evolutionary rescue. But extinction can result from failure to adapt not only to catastrophes, but also to a backlog of environmental challenges. We model long-term adaptation to long series of small challenges, where fitter populations reach higher population sizes. The population's long-term fitness dynamic is well approximated by a simple stochastic Markov chain model. Long-term persistence occurs when the rate of adaptation exceeds the rate of environmental deterioration for some genotypes. Long-term persistence times are consistent with typical fossil species persistence times of several million years. Immediately preceding extinction, fitness declines rapidly, appearing as though a catastrophe disrupted a stably established population, even though gradual evolutionary processes are responsible. New populations go through an establishment phase where, despite being demographically viable, their extinction risk is elevated. Should the population survive long enough, extinction risk later becomes constant over time.

Updating Darwin: Information and entropy drive the evolution of life

The evolution of species, according to Darwin, is driven by struggle – by competition between variant autonomous individuals for survival of the fittest and reproductive advantage; the outcome of this struggle for survival is natural selection. The Neo-Darwinians reframed natural selection in terms of DNA: inherited genotypes directly encode expressed phenotypes; a fit phenotype means a fit genotype – thus the evolution of species is the evolution of selfish, reproducing individual genotypes. Four general characteristics of advanced forms of life are not easily explained by this Neo-Darwinian paradigm: 1) Dependence on cooperation rather than on struggle, manifested by the microbiome, ecosystems and altruism; 2) The pursuit of diversity rather than optimal fitness, manifested by sexual reproduction; 3) Life’s investment in programmed death, rather then in open-ended survival; and 4) The acceleration of complexity, despite its intrinsic fragility. Here I discuss two mechanisms that can resolve these paradoxical features; both mechanisms arise from viewing life as the evolution of information. Information has two inevitable outcomes; it increases by autocatalyis and it is destroyed by entropy. On the one hand, the autocalalysis of information inexorably drives the evolution of complexity, irrespective of its fragility. On the other hand, only those strategic arrangements that accommodate the destructive forces of entropy survive – cooperation, diversification, and programmed death result from the entropic selection of evolving species. Physical principles of information and entropy thus fashion the evolution of life.

Association of a nonsynonymous substitution in the condensin NCAPG gene with traits of eggs in laying hens

One of the most important areas of research in the biology and genetics of farmed animals is one of identification of genes controlling the expression of traits with practical importance for animal breeding. For most of these characteristic features, the wide variation in gene expression in specific loci, which are called quantitative trait loci (QTL), is typical. Eggs have been researched for decades due to their importance for the reproduction of birds, as well as for its widespread use in pharmaceutical, cosmetic, and food industries. Breeding hens and crosslines are a necessary step for producing eggs with the desired quality. The results of this work are recommended for use to create systems of molecular markers for the marker selection of layers and obtain new lines and cross hens with larger mass eggs. Compared to the existing conventional systems of selecting layers on this basis, this will eliminate the assessment of the genotype of male progeny, which will significantly reduce breeding time. The system of markers will appear as a set of primers for detecting gene alleles that have a significant impact on the characteristics as above. The use of the molecular markers of high-performance systems for direct selection based on domestic chicken eggs should lead to substantial progress in biotechnology poultry and help avoid having to purchase similar systems from outside the country. The association of the condensin NCAPG gene with the egg traits of domestic chicken has been studied. Associations of the SNP alleles of the rs14491030 marker localized in exon 8 of the NCAPG gene with the trait “the weight eggs,” p < 0.001, as well as with the elastic deformation of the egg shell, p < 0.026, have been found. It has been found that a single nucleotide nonsynonymous A → G substitution leads to a significant increase in egg weight. The marker SNP rs14491030 with the observed significant effect on the egg weight trait can be recommended for use in breeding laying hens. The calculations of the relative fitness of genotypes of the SNP rs14491030 marker suggest a natural selection for heterozygotes. The results obtained are discussed in connection with the role of the canonical condensin complex in the compaction of chromatin and segregation of chromosomes.

Updating Darwin: Information and entropy drive the evolution of life.

The evolution of species, according to Darwin, is driven by struggle - by competition between variant autonomous individuals for survival of the fittest and reproductive advantage; the outcome of this struggle for survival is natural selection. The Neo-Darwinians reframed natural selection in terms of DNA: inherited genotypes directly encode expressed phenotypes; a fit phenotype means a fit genotype - thus the evolution of species is the evolution of selfish, reproducing individual genotypes. Four general characteristics of advanced forms of life are not easily explained by this Neo-Darwinian paradigm: 1) Dependence on cooperation rather than on struggle, manifested by the microbiome, ecosystems and altruism; 2) The pursuit of diversity rather than optimal fitness, manifested by sexual reproduction; 3) Life's investment in programmed death, rather then in open-ended survival; and 4) The acceleration of complexity, despite its intrinsic fragility. Here I discuss two mechanisms that can resolve these paradoxical features; both mechanisms arise from viewing life as the evolution of information. Information has two inevitable outcomes; it increases by autocatalyis and it is destroyed by entropy. On the one hand, the autocalalysis of information inexorably drives the evolution of complexity, irrespective of its fragility. On the other hand, only those strategic arrangements that accommodate the destructive forces of entropy survive - cooperation, diversification, and programmed death result from the entropic selection of evolving species. Physical principles of information and entropy thus fashion the evolution of life.