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PubMed1988

Genetics and demography in biological conservation.

Predicting the extinction of single populations or species requires ecological and evolutionary information. Primary demographic factors affecting population dynamics include social structure, life history variation caused by environmental fluctuation, dispersal in spatially heterogeneous environments, and local extinction and colonization. In small populations, inbreeding can greatly reduce the average individual fitness, and loss of genetic variability from random genetic drift can diminish future adaptability to a changing environment. Theory and empirical examples suggest that demography is usually of more immediate importance than population genetics in determining the minimum viable sizes of wild populations. The practical need in biological conservation for understanding the interaction of demographic and genetic factors in extinction may provide a focus for fundamental advances at the interface of ecology and evolution.

Animals↗
PubMed1998

Sustainability of transgenic insecticidal cultivars: integrating pest genetics and ecology.

This review examines potential impacts of transgenic cultivars on insect population dynamics and evolution. Experience with classically bred, insecticidal cultivars has demonstrated that a solid understanding of both the target insect's ecology and the cultivar's performance under varied field conditions will be essential for predicting area-wide effects of transgenic cultivars on pest and natural enemy dynamics. This experience has also demonstrated the evolutionary capacity of pests for adaptive response to insecticidal traits in crops. Biochemical and genetic studies of insect adaptation to the Bacillus thuringiensis (Bt) toxins expressed by currently marketed transgenic cultivars indicate a high risk for rapid adaptation if these cultivars are misused. Theoretical and practical issues involved in implementing strategies to delay pest adaptation to insecticidal cultivars are reviewed. Emphasis is placed on examining the "high dose"/refuge strategy that has become the goal of industry and regulatory authorities.

Journal Article↗
PubMed2003

Evolving small neurocontrollers with self-organized compact encoding.

This article presents a novel method for the evolution of artificial autonomous agents with small neurocontrollers. It is based on adaptive, self-organized compact genotypic encoding (SOCE) generating the phenotypic synaptic weights of the agent's neurocontroller. SOCE implements a parallel evolutionary search for neurocontroller solutions in a dynamically varying and reduced subspace of the original synaptic space. It leads to the emergence of compact successful neurocontrollers starting from large networks. The method can serve to estimate the network size needed to perform a given task, and to delineate the relative importance of the neurons composing the agent's controller network.

Evolution, Molecular↗
PubMed2026

Repair and regeneration across the lifespan: an ontogenetic perspective.

The capacity for tissue repair and regeneration undergoes a profound and progressive decline across the human lifespan, representing a fundamental driver of aging and chronic disease. This review establishes a comprehensive ontogenetic framework by mapping the continuous biological transition from the flawless, scarless regenerative plasticity of embryonic development to the irreversible fibrotic scarring and organ failure characteristic of senescence. We synthesize the hierarchical collapse of reparative networks across multiple biological scales. Importantly, this ontogenetic decline should not be interpreted as a purely degenerative trajectory but rather as a dynamic systems-level reprogramming in which evolutionary trade-offs prioritize tumor suppression, immune surveillance, and reproductive fitness over long-term regenerative fidelity. Recognizing this adaptive reallocation of biological resources reframes aging not simply as failure but as a predictable recalibration of repair hierarchies. At the molecular and cellular levels, the accumulation of genomic instability, unresolvable DNA damage, and mitochondrial dysfunction gradually overwhelms intracellular quality-control mechanisms. Concurrently, epigenetic drift and chronic, low-grade systemic inflammation ("inflammaging") dismantle the stem cell niche, driving adult stem cell exhaustion and shifting wound healing away from functional tissue replacement toward maladaptive fibrosis. Furthermore, we examine divergent, organ-specific repair trajectories. By contrasting the severe regenerative restrictions of the adult central nervous system and myocardium with the persistent, yet exhaustible, resilience of the liver, we elucidate the unique intrinsic and microenvironmental barriers that impede structural and functional recovery. Finally, we evaluate the clinical paradigm shift from passive management of age-related degeneration to active restoration of tissue integrity. By integrating systemic geroscience-which addresses the global hallmarks of aging-with targeted bioengineering and in vivo epigenetic modulation, contemporary regenerative medicine seeks to recreate permissive, youthful microenvironments. Ultimately, mastering these ontogenetic principles holds unprecedented potential to reactivate endogenous repair pathways, mitigate multi-organ collapse, and significantly extend human functional healthspan.

DNA repair↗
PubMed2004

Experimental evidence for sympatric ecological diversification due to frequency-dependent competition in Escherichia coli.

We investigate adaptive diversification in experimental Escherichia coli populations grown in serial batch cultures on a mixture of glucose and acetate. All 12 experimental lines were started from the same genetically uniform ancestral strain but became highly polymorphic for colony size after 1000 generations. Five populations were clearly dimorphic and thus serve as a model for an adaptive lineage split. We analyzed the ecological basis for this dimorphism by studying bacterial growth curves. All strains exhibit diauxie, that is, sequential growth on the two resources. Thus, they exhibit phenotypic plasticity, using mostly glucose when glucose is abundant, then switching to acetate when glucose concentration is low. However, the coexisting strains differ in their diauxie pattern, with one cluster in the dimorphic populations growing better in the glucose phase, and the other cluster having a much shorter lag when switching to the acetate phase. Using invasion experiments, we show that the dimorphism of these two ecological types is maintained by frequency-dependent selection. Using a mathematical model for the adaptive dynamics of diauxie behavior, we show that evolutionary branching in diauxie behavior is a plausible theoretical scenario. Our results support the hypothesis that, in our experiments, adaptive diversification from a genetically uniform ancestor occurred due to frequency-dependent ecological interactions. Our results have implications for understanding the evolution of cross-feeding polymorphism in microorganisms, as well as adaptive speciation due to frequency-dependent selection on phenotypic plasticity.

Adaptation, Physiological↗
PubMed1985

Comparison of MHC genes among distantly related members of the genus Mus.

The genomic content of class I and class II MHC DNA sequences in a variety of wild mice has been analyzed. The panel of mice includes members of three subgenera of the genus Mus. By genomic hybridization with the use of a variety of DNA probes, both class I and class II DNA sequences appear to be conserved in all of the species examined. However, the number of class I DNA sequences differs among the species. Furthermore, this variation appears to result from differential increases within subsets of class I genes. These data suggest that the class I multigene family is dynamic and changing over short periods of evolutionary time. In contrast, none of the class II genes appears to vary in copy number. More extensive polymorphism was noted amongst the class II beta genes than the alpha genes. Interestingly, the genomic sequence corresponding to E beta 2 is highly conserved, leading to the prediction that it is a genetically functional sequence.

Animals↗
PubMed1997

Dynamics of the emergence of genetic resistance to biocides among asexual and sexual organisms.

A stochastic, agent based, evolutionary algorithm, modeling mating, reproduction, genetic variation, phenotypic expression and selection was used to study the dynamic interactions affecting a multiple-gene system. The results suggest that strong irreversible constraints affect the evolution of resistance to biocides. Resistant genes evolve differently in asexual organisms compared with sexual ones in response to various patterns of biocide applications. Asexual populations (viruses and bacteria) are less likely to develop genetic resistance in response to multiple pesticides or if pesticides are used at low doses, whereas sexual populations (insects for example) are more likely to become resistant to pesticides if susceptibility to the pesticide relates to mate selection. The adaptation of genes not related to the emergence of resistance will affect the dynamics of the evolution of resistance. Increasing the number of pesticides reduces the probability of developing resistance to any of them in asexual organisms but much less so in sexual organisms. Sequential applications of toxins, were slightly less efficient in slowing emergence of resistance compared with simultaneous application of a mix in both sexual and asexual organisms. Targeting only one sex of the pest speeds the development of resistance. The findings are consistent to most of the published analytical models but are closer to known experimental results, showing that nonlinear, agent based simulation models are more powerful in explaining complex processes.

Algorithms↗
PubMed2000

Adaptive feeding across environmental gradients and its effect on population dynamics.

This paper analyzes a consumer's adaptive feeding response to environmental gradients. We consider a consumer-resource system where resources are distributed among many discrete resource patches. Each consumer exhibits a feeding morphology allowing it to remove resources from a patch down to some threshold density (or level) before having to seek resources elsewhere. Assuming consumers trade off resource extraction with patch access and predation, we show that for a given environment there often exists a single evolutionarily stable feeding threshold and it is an evolutionary attractor. We then investigate how the population dynamics of the resource and the consumer change as the environment changes. Two cases are considered: (i) all consumers exhibit a fixed feeding threshold that is adaptive for an intermediate environment; and (ii) the consumer population adapts and adopts the evolutionarily stable feeding threshold associated with the current environment. In less harsh environments (i.e., environments where consumers experience a lower risk of predation, or environments where resource patches are more abundant) the adaptive consumer population is predicted to evolve so that resources within a patch are depleted to lower densities. We show that the change in consumer density due to environmental change can be rather different depending on whether or not the population can adapt. In some situations we observe that when the consumer's environment becomes harsher, the consumer population may increase in density before a rapid crash to extinction. This result has implications for monitoring and managing a population.

Adaptation, Physiological↗
PubMed2007

Resolving the tragedy of the commons: the feedback between intraspecific conflict and population density.

Competition and conflict among individuals can favour exploitative strategies that undermine the common good. Theory suggests that this can lead to a tragedy of the commons and ultimately population extinction, a phenomenon known as evolutionary suicide. Here, I present a model of the evolutionary tragedy of the commons that explicitly considers the population dynamics where individuals invest in individually costly competitive traits. In the simplest form, this supports the notion that selection for high levels of conflict can cause evolutionary suicide. However, as competition comes with survival and fecundity costs, a feedback between the investment in competition and population density can act to reduce the level of conflict and prevent the population from going extinct. This suggests that the interaction between population ecology and the evolution of competition and conflict among individuals may be an important mechanism in resolving the level of competition and conflict among individuals.

Biological Evolution↗
PubMed2006

Evaluation of models for the evolution of protein sequences and functions under structural constraint.

In the field of evolutionary structural genomics, methods are needed to evaluate why genomes evolved to contain the fold distributions that are observed. In order to study the effects of population dynamics in the evolved genomes we need fast and accurate evolutionary models which can analyze the effects of selection, drift and fixation of a protein sequence in a population that are grounded by physical parameters governing the folding and binding properties of the sequence. In this study, various knowledge-based, force field, and statistical methods for protein folding have been evaluated with four different folds: SH2 domains, SH3 domains, Globin-like, and Flavodoxin-like, to evaluate the speed and accuracy of the energy functions. Similarly, knowledge-based and force field methods have been used to predict ligand binding specificity in SH2 domain. To demonstrate the applicability of these methods, the dynamics of evolution of new binding capabilities by an SH2 domain is demonstrated.

Computational Biology↗
PubMed2000

Population cycles caused by selection by density dependent competitive interactions.

Several animal species have cyclic population dynamics with phase-related cycles in life history traits such as body mass, reproductive rate, and pre-reproductive period. Although many mechanisms have been proposed there is no agreement on the cause of these cycles, and no population equation that deduces both the abundance and the life history cycles from basic ecological constraints has been formulated. Here I deduce a population dynamic equation from the selection pressure of density dependent competitive interactions in order to explain the cyclic dynamics in abundance and life history traits. The model can explain cycles by evolutionary changes in the genotype or by plastic responses in the phenotype. It treats the population dynamic growth rate as an initial condition, and its density independent fundament is Fisher's (1930, The Genetical Theory of Natural Selection, Oxford: Clarendon) fundamental theorem of natural selection that predicts a hyper-geometrical increase in abundance. The predicted periods coincide with the cyclic dynamics of Lepidoptera, and the Calder hypothesis, which suggests that the period of population cycles is proportional to the 1/4 power of body mass, follows from first principles of the proposed density dependent ecology.

Animals↗
PubMed2005

Mutation in evolutionary games can increase average fitness at equilibrium.

We study game dynamical interactions between two strategies, A and B, and analyse whether the average fitness of the population at equilibrium can be increased by adding mutation from A to B. Classifying all two by two games with payoff matrix [(a,b),(c,d)], we show that mutation from A to B enhances the average fitness of the whole population (i) if both a and d are less than (b + c)/2 and (ii) if c is less than b. Furthermore, we study conditions for maximizing the productivity of strategy A, and we analyse the effect of mutations in both directions. Depending on the biological system, a mutation in an evolutionary game can be interpreted as a genetic alteration, a cellular differentiation, a change in gene expression, an accidental or deliberate modification in cultural transmission, or a learning error. In a cultural context, our results indicate that the equilibrium payoff of the population can be increased if players sometimes choose the strategy with lower payoff. In a genetic context, we have shown that for frequency-dependent selection mutation can enhance the average fitness of the population at equilibrium.

Animals↗
PubMed2026

Evolutionary diversification of invertase paralogs couples carbon metabolism and sexual reproduction in fission yeasts.

Dynamic patterns of gene gain and loss play a major role in the diversification of eukaryotes, reflecting adaptation to a broad range of ecological contexts. Reconstructing the evolutionary history of genes provides a powerful framework for understanding how functional innovation shapes life-history traits. Here we report a comprehensive analysis of gene gain and loss across the fission yeast clade, whose evolutionary trajectory remains elusive. Reductive evolution of metabolic genes is a major contributor to species diversification, as observed in other fungal taxa. Notably, we uncovered an evolutionary scenario in which an ancestral gene duplication was followed by lineage-specific loss of one or the other paralog, except in S. pombe, which retained both. We demonstrate that these paralogs encode catalytically-active invertases, named Inv1 and Inv2, with distinct enzymatic properties, localization, regulation, and physiological roles. Inv1 is a secreted enzyme subject to glucose catabolite repression and is the sole invertase required for sucrose assimilation, resembling canonical yeast invertases. In contrast, Inv2 is intracellular, constitutively expressed, and required for inducing sexual differentiation in response to nutrient availability. Overall, these findings reveal an unexpected role for carbon metabolism in modulating the haploid-diploid cycle of fission yeasts, suggesting that diversification of core metabolic functions may contribute to adaptation to environments with distinct sugar compositions.

Evolution↗
PubMed1996

Genetic versus phenotypic models of selection: can genetics be neglected in a long-term perspective?

Game theoretical concepts in evolutionary biology have been criticized by populations geneticists, because they neglect such crucial aspects as the mating system or the mode of inheritance. In fact, the dynamics of natural selection does not necessarily lead to a fitness maximum or an ESS if genetic constraints are taken into account. Yet, it may be premature to conclude that game theoretical concepts do not have a dynamical justification. The new paradigm of long-term evolution postulates that genetic constraints, which may be dominant in a short-term perspective, will in the long run disappear in the face of the ongoing influx of mutations. Two basic results (see Hammerstein; this issue) seem to reconcile the dynamical approach of long-term population genetics with the static approach of evolutionary game theory: (1) only populations at local fitness optima (Nash strategies) can be long-term stable; and (2) in monomorphic populations, evolutionary stability is necessary and sufficient to ensure long-term dynamic stability. The present paper has a double purpose. On the one hand, it is demonstrated by fairly general arguments that the scope of the results mentioned above extends to non-linear frequency dependent selection, to multiple loci, and to quite general mating systems. On the other hand, some limitations of the theory of long-term evolution will also be stressed: (1) there is little hope for a game theoretical characterization of stability in polymorphic populations; (2) many interesting systems do not admit long-term stable equilibria; and (3) even if a long-term stable equilibrium exists, it is not at all clear whether and how it is attainable by a series of gene substitution events.

Biological Evolution↗
PubMed2005

Spatio-temporal dynamics of the visual system revealed in binocular rivalry.

From the evolutionary viewpoint, animals need to monitor the surrounding environment and capture salient features, such as motion, for survival. The visual system is highly developed for monitoring a wide area of visual field and capturing such salient features. In humans and primates, there is a wide binocular field, suggesting a necessity of integrating the images from the two eyes. Binocular rivalry [R. Blake, A neural theory of binocular rivalry, Psychol. Rev. 96 (1989) 145-167; R. Blake, N.K. Logothetis, Visual competition, Nat. Rev. Neurosci. 3 (2002) 13-21], where incompatible inputs from the two eyes compete to emerge in the subject's visual percept, has been shown to exhibit highly adaptive behavior [I. Kovacs, T.V. Parathomas, M. Yang, A. Feher, When the brain changes its mind: interocular grouping during binocular rivalry. Proc. Natl. Acad. Sci. U.S.A. 93 (1996) 15508-15511; N.K. Logothetis, Single units and conscious vision, Philos. Trans. R. Soc. Lond. B. Biol. Sci. 353 (1998) 1801-1818]. Here we investigated the spatio-temporal dynamics of the ocular dominance pattern in binocular rivalry under conditions where conflicting salient features were presented in a temporally varying manner. We found a striking example of the detailed structure of the dominance wave propagation, by using a spatio-temporal sampling method. The data show in detail the ability of the visual system to dynamically adapt to the changing stimuli in the context of the massively parallel visual field. We show by model prediction that the globally coherent dominance change in the presence of multiple stimuli can be explained by a mechanism based on local saliency comparison.

Adaptation, Physiological↗
PubMed2000

Trophic-dynamic considerations in relating species diversity to ecosystem resilience.

Complexity in the networks of interactions among and between the living and abiotic components forming ecosystems confounds the ability of ecologists to predict the economic consequences of perturbations such as species deletions in nature. Such uncertainty hampers prudent decision making about where and when to invest most intensively in species conservation programmes. Demystifying ecosystem responses to biodiversity alterations may be best achieved through the study of the interactions allowing biotic communities to compensate internally for population changes in terms of contributing to ecosystem function, or their intrinsic functional redundancy. Because individual organisms are the biologically discrete working components of ecosystems and because environmental changes are perceived at the scale of the individual, a mechanistic understanding of functional redundancy will hinge upon understanding how individuals' behaviours influence population dynamics in the complex community setting. Here, I use analytical and graphical modelling to construct a conceptual framework for predicting the conditions under which varying degrees of interspecific functional redundancy can be found in dynamic ecosystems. The framework is founded on principles related to food web successional theory, which provides some evolutionary insights for mechanistically linking functional roles of discrete, interacting organisms with the dynamics of ecosystems because energy is the currency both for ecological fitness and for food web commerce. Net productivity is considered the most contextually relevant ecosystem process variable because of its socioeconomic significance and because it ultimately subsumes all biological processes and interactions. Redundancy relative to productivity is suggested to manifest most directly as compensatory niche shifts among adaptive foragers in exploitation ecosystems, facilitating coexistence and enhancing ecosystem recovery after disturbances which alter species' relative abundances, such as extinctions. The framework further explicates how resource scarcity and environmental stochasticity may constitute 'ecosystem legacies' influencing the emergence of redundancy by shaping the background conditions for foraging behaviour evolution and, consequently, the prevalence of compensatory interactions. Because it generates experimentally testable predictions for a priori hypothesis testing about when and where varying degrees of functional redundancy are likely to be found in food webs, the framework may be useful for advancing toward the reliable knowledge of biodiversity and ecosystem function relations necessary for prudent prioritization of conservation programmes. The theory presented here introduces explanation of how increasing diversity can have a negative influence on ecosystem sustainability by altering the environment for biotic interactions and thereby changing functional compensability among biota--under particular conditions.

Animals↗
PubMed2006

Low-frequency normal modes that describe allosteric transitions in biological nanomachines are robust to sequence variations.

By representing the high-resolution crystal structures of a number of enzymes using the elastic network model, it has been shown that only a few low-frequency normal modes are needed to describe the large-scale domain movements that are triggered by ligand binding. Here we explore a link between the nearly invariant nature of the modes that describe functional dynamics at the mesoscopic level and the large evolutionary sequence variations at the residue level. By using a structural perturbation method (SPM), which probes the residue-specific response to perturbations (or mutations), we identify a sparse network of strongly conserved residues that transmit allosteric signals in three structurally unrelated biological nanomachines, namely, DNA polymerase, myosin motor, and the Escherichia coli chaperonin. Based on the response of every mode to perturbations, which are generated by interchanging specific sequence pairs in a multiple sequence alignment, we show that the functionally relevant low-frequency modes are most robust to sequence variations. Our work shows that robustness of dynamical modes at the mesoscopic level is encoded in the structure through a sparse network of residues that transmit allosteric signals.

Allosteric Regulation↗
PubMed2006

indel-Seq-Gen: a new protein family simulator incorporating domains, motifs, and indels.

Reconstructing the evolutionary history of protein sequences will provide a better understanding of divergence mechanisms of protein superfamilies and their functions. Long-term protein evolution often includes dynamic changes such as insertion, deletion, and domain shuffling. Such dynamic changes make reconstructing protein sequence evolution difficult and affect the accuracy of molecular evolutionary methods, such as multiple alignments and phylogenetic methods. Unfortunately, currently available simulation methods are not sufficiently flexible and do not allow biologically realistic dynamic protein sequence evolution. We introduce a new method, indel-Seq-Gen (iSG), that can simulate realistic evolutionary processes of protein sequences with insertions and deletions (indels). Unlike other simulation methods, iSG allows the user to simulate multiple subsequences according to different evolutionary parameters, which is necessary for generating realistic protein families with multiple domains. iSG tracks all evolutionary events including indels and outputs the "true" multiple alignment of the simulated sequences. iSG can also generate a larger sequence space by allowing the use of multiple related root sequences. With all these functions, iSG can be used to test the accuracy of, for example, multiple alignment methods, phylogenetic methods, evolutionary hypotheses, ancestral protein reconstruction methods, and protein family classification methods. We empirically evaluated the performance of iSG against currently available methods by simulating the evolution of the G protein-coupled receptor and lipocalin protein families. We examined their true multiple alignments, reconstruction of the transmembrane regions and beta-strands, and the results of similarity search against a protein database using the simulated sequences. We also presented an example of using iSG for examining how phylogenetic reconstruction is affected by high indel rates.

Carrier Proteins↗