The devolution of evolution.
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Adaptation, Biological↗
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Molecular evolution of human visual pigment genes.
By comparing the published DNA sequences for (a) the genes encoding the human visual color pigments (red, green, and blue) with (b) the genes encoding human, bovine, and Drosophila rhodopsins, a phylogenetic tree for the mammalian pigment genes has been constructed. This evolutionary tree shows that the common ancestor of the visual color pigment genes diverged first from that of the rhodopsin genes; then the common ancestor of the red and green pigment genes and the ancestor of the blue pigment gene diverged; and finally the red and green pigment genes diverged from each other much more recently. Nucleotide substitutions in the rhodopsin genes are best explained by the neutral theory of molecular evolution. However, important functional adaptations seem to have occurred twice during the evolution of the color pigment genes in humans: first, to the common ancestor of the three color pigment genes after its divergence from the ancestor of the rhodopsin gene and, second, to the ancestor of the red pigment gene after its divergence from that of the green pigment gene.
Amino Acid Sequence↗
Happy together: the life and times of Ty retrotransposons and their hosts.
The aim of this review is to describe the level of intimacy between Ty retrotransposons (Ty1-Ty5) and their host the yeast Saccharomyces cerevisiae. The effects of Ty location in the genome and of host proteins on the expression and mobility of Ty elements are highlighted. After a brief overview of Ty diversity and evolution, we describe the factors that dictate Ty target-site preference and the impact of targeting on Ty and adjacent gene expression. Studies on Ty3 and Ty5 have been especially informative in unraveling the role of host factors (Pol III machinery and silencing proteins, respectively) and integrase in controlling the specificity of integration. In contrast, not much is known regarding Ty1, Ty2 and Ty4, except that their insertion depends on the transcriptional competence of the adjacent Pol III gene and might be influenced by some chromatin components. This review also brings together recent findings on the regulation of Ty1 retrotransposition. A large number of host proteins (over 30) involved in a wide range of cellular processes controls either directly or indirectly Ty1 mobility, primarily at post-transcriptional steps. We focus on several genes for which more detailed analyses have permitted the elaboration of regulatory models. In addition, this review describes new data revealing that repression of Ty1 mobility also involves two forms of copy number control that act at both the trancriptional and post-transcriptional levels. Since S. cerevisiae lacks the conserved pathways for copy number control via transcriptional and post-transcriptional gene silencing found in other eukaryotes, Ty1 copy number control must be via another mechanism whose features are outlined. Ty1 response to stress also implicates activation at both transcriptional and postranscriptional steps of Ty1. Finally, we provide several insights in the role of Ty elements in chromosome evolution and yeast adaptation and discuss the factors that might limit Ty ectopic recombination.
Evolution, Molecular↗
Dynamics of competing species in a model of adaptive radiation and macroevolution.
We present a simple model of adaptive radiation in evolution based on species competition. Competition is found to promote species divergence and branching, and to dampen the net species production. In the model simulations, high taxonomic diversification and branching take place during the beginning of the radiation. The results show striking similarities with empirical data and highlight the mechanism of competition as an important driving factor for accelerated evolutionary transformation.
Adaptation, Physiological↗
Are we eating more than we think? Illegitimate signaling and xenohormesis as participants in the pathogenesis of obesity.
Resource utilization may represent a central force driving evolution. A tight link between sensing energy availability and managing energy acquisition and utilization constitutes a common feature among all organisms. While such a link was likely adaptive during prehistoric evolution, modern lifestyles may decouple perceived cues from actual energy availability so as to promote obesity in humans. A particular illegitimate signal is chronic stress, which may shift body phenotype to suit a more conservative state of energy management. In prehistoric times, such a response likely aided survival during periods of low resource availability. However, new sources of chronic stress have emerged that bear little relationship to contextual energy, which is generally abundant in the modern world. In addition, modern techniques of husbandry and agriculture can produce stress in the food chain, such that food itself can act as an illegitimate signal of chronic stress. Obese livestock and unusual fat profiles in farmed fish, meat, and eggs may reflect stress phenotypes. Consumers of stressed foods may sense those signals--a phenomenon known as xenohormesis--and assume the stressed phenotype. This maladaptive process may promote obesity by erroneously biasing hosts towards caloric accumulation in the context of energy abundance. Regional tissue accumulation of fat may indicate local tissue stress. Atherosclerosis may result from stress signals that induce sympathetic bias and regional fat accumulation in vessel adventitia. Medications such as neuroleptics and foods such as diet drinks may generate illegitimate signals by mimicking molecules used for energy management. Implications for the prevention and treatment of dysfunctions related to these derangements are discussed. New strategies for manufacturing biologics by manipulating stress conditions or controlling fatty acid attachments to proteins are envisioned.
Adipose Tissue↗
Parallel evolution of chimeric fusion genes.
To understand how novel functions arise, we must identify common patterns and mechanisms shaping the evolution of new genes. Here, we take advantage of data from three Drosophila genes, jingwei, Adh-Finnegan, and Adh-Twain, to find evolutionary patterns and mechanisms governing the evolution of new genes. All three of these genes are independently derived from Adh, which enabled us to use the extensive literature on Adh in Drosophila to guide our analyses. We discovered a fundamental similarity in the temporal, spatial, and types of amino acid changes that occurred. All three genes underwent rapid adaptive amino acid evolution shortly after they were formed, followed by later quiescence and functional constraint. These genes also show striking parallels in which amino acids change in the Adh region. We showed that these early changes tend to occur at amino acid residues that seldom, if ever, evolve in Drosophila Adh. Changes at these slowly evolving sites are usually associated with loss of function or hypomorphic mutations in Drosophila melanogaster. Our data indicate that shifting away from ancestral functions may be a critical step early in the evolution of chimeric fusion genes. We suggest that the patterns we observed are both general and predictive.
Adaptation, Biological↗
Evolution of catabolic pathways and metabolic versatility in Pseudomonas stutzeri OX1.
Pseudomonas stutzeri OX1 is able to degrade toluene and ortho-xylene via the direct oxygenation of the aromatic ring. The genetic studies carried out suggest that the genes coding for the monooxygenase involved in the early steps of this catabolic route have been acquired by gene transfer. P stutzeri OX1 is also potentially able to utilize meta- and para-xylene as growth substrates. These two isomers are metabolized through a different pathway (TOL pathway). Both catabolic routes can be activated or inactivated by means of genomic rearrangements. The relevance of such recombination mechanisms in the evolution and the adaptability of P. stutzeri is discussed.
Biodegradation, Environmental↗
Roles of E. coli double-strand-break-repair proteins in stress-induced mutation.
Special mechanisms of mutation are induced during growth-limiting stress and can generate adaptive mutations that permit growth. These mechanisms may provide improved models for mutagenesis in antibiotic resistance, evolution of pathogens, cancer progression and chemotherapy resistance. Stress-induced reversion of an Escherichia coli episomal lac frameshift allele specifically requires DNA double-strand-break-repair (DSBR) proteins, the SOS DNA-damage response and its error-prone DNA polymerase, DinB. We distinguished two possible roles for the DSBR proteins. Each might act solely upstream of SOS, to create single-strand DNA that induces SOS. This could upregulate DinB and enhance mutation globally. Or any or all of them might function other than or in addition to SOS promotion, for example, directly in error-prone DSBR. We report that in cells with SOS genes derepressed constitutively, RecA, RuvA, RuvB, RuvC, RecF, and TraI remain required for stress-induced mutation, demonstrating that these proteins act other than via SOS induction. RecA and TraI also act by promoting SOS. These and additional results with hyper-mutating recD and recG mutants support roles for these proteins via error-prone DSBR. Such mechanisms could localize stress-induced mutagenesis to small genomic regions, a potentially important strategy for adaptive evolution, both for reducing additional deleterious mutations in rare adaptive mutants and for concerted evolution of genes.
Alleles↗
Adaptive dynamics in diploid, sexual populations and the evolution of reproductive isolation.
Evolutionary branching is the process whereby an initially monomorphic population evolves to a point where it undergoes disruptive selection and splits up into two phenotypically diverging lineages. We studied evolutionary branching in three models that are ecologically identical but that have different genetic systems. The first model is clonal, the second is sexual diploid with additive genetics on a single locus and the third is like the second but with an additional locus for mate choice. Evolutionary branching occurred under exactly the same ecological circumstances in all three models. After branching the evolutionary dynamics may be qualitatively different. In particular, in the diploid, sexual models there can be multiple evolutionary outcomes whereas in the corresponding clonal model there is only one. We showed that evolutionary branching favours the evolution of (partial) assortative mating and that this in turn effectively restores the results from the clonal model by rendering the alternative outcomes unreachable except for the one that also occurs in the clonal model. The evolution of assortative mating during evolutionary branching can be interpreted as the initial phase of sympatric speciation with phenotypic divergence and partial reproductive isolation.
Adaptation, Physiological↗
Adaptive host preference and the dynamics of host-parasitoid interactions.
Models of two independent host populations and a common parasitoid are investigated. The hosts have density-dependent population growth and only interact indirectly by their effects on parasitoid behavior and population dynamics. The parasitoid is assumed to experience a trade-off in its ability to exploit the two hosts. Three alternative types of parasitoid are investigated: (i) fixed generalists whose consumption rates are those that maximize fitness; (ii) "ideal free" parasitoids, which modify their behavior to maximize their rate of finding unparasitized hosts within a generation; and (iii) "evolving" parasitoids, whose capture rates change between generations based on quantitative genetic determination of the relative attack rates on the two hosts. The primary questions addressed are: (1) Do the different types of adaptive processes stabilize or destabilize the population dynamics? (2) Do the adaptive processes tend to equalize or to magnify differences in host densities? The models show that adaptive behavior and evolution frequently destabilize population dynamics and frequently increase the average difference between host densities.
Adaptation, Biological↗
Evolution: the evolvability enigma.
A report that a switch of a yeast protein to a 'prion' state triggers diverse phenotypic changes has prompted re-examination of the processes of evolution. To what extent should processes of gene expression and control be interpreted in terms of their capacity to allow future evolution as well as present adaptation?
Adaptation, Physiological↗
Removing irrelevant features in neural network classification using evolutionary computations.
Evolutionary artificial neural networks (EANN) are a new paradigm that refers to a special class of artificial neural networks (ANN) in which evolution is another fundamental form of adaptation in addition to learning. Evolution can be introduced at various levels of ANN. It can be used to evolve weights, architectures and learning parameters. Evolutionary computations are population-based search methods that have shown promise in many similarly complex tasks. This paper presents an application of evolutionary programming for simultaneously inducing the input structure and weights evolving for multilayer feed-forward perceptrons (MLP) with standard sigmoidal activation function.
Algorithms↗
Xist and the order of silencing.
X inactivation is the mechanism by which mammals adjust the genetic imbalance that arises from the different numbers of gene-rich X-chromosomes between the sexes. The dosage difference between XX females and XY males is functionally equalized by silencing one of the two X chromosomes in females. This dosage-compensation mechanism seems to have arisen concurrently with early mammalian evolution and is based on the long functional Xist RNA, which is unique to placental mammals. It is likely that previously existing mechanisms for other cellular functions have been recruited and adapted for the evolution of X inactivation. Here, we critically review our understanding of dosage compensation in placental mammals and place these findings in the context of other cellular processes that intersect with mammalian dosage compensation.
Animals↗
Metabolic convergence of diabetes and prostate cancer: from dysglycemia to tumor microenvironment reprogramming.
The relationship between diabetes mellitus and prostate cancer (PC) represents one of the most intriguing paradoxes in cancer epidemiology, with diabetic individuals exhibiting a reduced incidence of PC yet poorer prognosis following diagnosis. This apparent contradiction underscores the need for an integrated understanding of how systemic metabolic dysfunction influences prostate carcinogenesis and disease progression. The present review critically synthesizes contemporary epidemiological, mechanistic, and translational evidence to establish metabolic convergence as a unifying framework linking diabetes-associated metabolic abnormalities with PC biology. Current evidence indicates that chronic dysglycemia, hyperinsulinemia, insulin resistance, and endocrine perturbations orchestrate interconnected intracellular signaling networks involving PI3K-AKT-mTOR, AMPK, AGE-RAGE signaling, oxidative stress, mitochondrial dysfunction, and epigenetic reprogramming, collectively driving metabolic adaptation and tumor evolution. Beyond tumor-intrinsic mechanisms, diabetes profoundly remodels the prostate tumor microenvironment through alterations in stromal metabolism, cancer-associated fibroblast activation, adipocyte-tumor crosstalk, extracellular matrix (ECM) remodeling, hypoxic adaptation, and vascular dysfunction, while simultaneously promoting immunometabolic reprogramming characterized by macrophage polarization, T-cell dysfunction, immune checkpoint activation, and immune evasion. The review further examines the bidirectional interactions between antidiabetic therapies and PC treatment, critically evaluating the translational potential of metformin and emerging glucose-lowering agents within the context of precision metabolic therapeutics. Finally, future directions encompassing biomarker-guided patient stratification, longitudinal metabolic profiling, multi-omics integration, artificial intelligence, and clinically relevant mechanistic validation are discussed as essential components of next-generation precision oncology. Collectively, this review reframes diabetes as an active metabolic determinant of PC rather than a coincidental comorbidity and highlights metabolism-centered precision strategies as promising avenues for improving risk stratification, therapeutic decision-making, and clinical outcomes in diabetes-associated PC.
Humans↗
Training improves the adaptation to changing visual conditions in maintaining human posture control in a test of sinusoidal oscillation of the support.
Balance control relies on somesthetic, visual and vestibular afferences, their central processing, and adequate motor responses. We studied the consequences on postural control of the suppression of visual afferences by eye closure, during a dynamic posturographic test in six sportsmen and 14 non-sportsmen. Suppression of visual afferences during the test led to a prolongation of the pattern initially recorded with eyes open, followed by a transitory adaptive pattern, then a typical eyes closed pattern. Repetition of the test showed a progressively longer persistence of the eyes open pattern and disappearance of the adaptive one. This evolution was significantly faster in sportsmen. This progressively longer duration of the eyes open pattern may be explained by the intervention of short term memory. Our data further indicate that training improves adaptive posture control.
Adult↗
Gene flow maintains a large genetic difference in clutch size at a small spatial scale.
Understanding the capacity of natural populations to adapt to their local environment is a central topic in evolutionary biology. Phenotypic differences between populations may have a genetic basis, but showing that they reflect different adaptive optima requires the quantification of both gene flow and selection. Good empirical data are rare. Using data on a spatially structured island population of great tits (Parus major), we show here that a persistent difference in mean clutch size between two subpopulations only a few kilometres apart has a major genetic component. We also show that immigrants from outside the island carry genes for large clutches. But gene flow into one subpopulation is low, as a result of a low immigration rate together with strong selection against immigrant genes. This has allowed for adaptation to the island environment and the maintenance of small clutches. In the other area, however, higher gene flow prevents local adaptation and maintains larger clutches. We show that the observed small-scale genetic difference in clutch size is not due to divergent selection on the island, but to different levels of gene flow from outside the island. Our findings illustrate the large effect of immigration on the evolution of local adaptations and on genetic population structure.
Animal Migration↗
[Current concept of scientific pharmacotherapy. Role of nutrition in the regulation of body's vital activity and homeostasis].
Drugs affect all the body's living physiological systems: cells, tissues, organs, organism as a whole but not alone, but in combination with all substances and trace elements accumulated in the body in the interaction with the environment, mainly from the ingested foods, water, drinks, ready-made industrial foodstuffs containing food additives. Food is a drug precursor (prodrug) and requires methods used in the study of the quality of combined drugs. During evolution, man has adapted himself to the intake of a complex of components of ecology surrounding him in his whole life. All the intrinsic mechanisms of life (the construction of cellular membranes (the soft skeleton), the provision of cell and tissue performance, the metabolism of substances and energy) are interrelated by special regulatory molecular and biochemical systems which ensures the constancy of vital activities, the renewal of fluids and cells (homeostasis). The Russian foodstuffs are the most optimum to promote health and to create a favourable background for the effects of drugs, in particular Russian drugs which the population has adapted itself to. The development of manufacture of natural drugs, those of plant and biotechnological origin is promising. Natural varying food and goal-oriented biotechnological foods create a base for normal evolution, health promotion, prophylaxis and treatment in man with drugs and non-drugs.
Drug Therapy↗
Modeling adaptive biological systems.
During the evolution of many systems found in nature, both the system composition and the interactions between components will vary. Equating the dimension with the number of different components, a system which adds or deletes components belongs to a class of dynamical systems with a finite dimensional phase space of variable dimension. We present two models of biochemical systems with a variable phase space, a model of autocatalytic reaction networks in the prebiotic soup and a model of the idiotypic network of the immune system. Each model contains characteristic meta-dynamical rules for constructing equations of motion from component properties. The simulation of each model occurs on two levels. On one level, the equations of motion are integrated to determine the state of each component. On a second level, algorithms which approximate physical processes in the real system are employed to change the equations of motion. Models with meta-dynamical rules possess several advantages for the study of evolving systems. First, there are no explicit fitness functions to determine how the components of the model rank in terms of survivability. The success of any component is a function of its relationship to the rest of the system. A second advantage is that since the phase space representation of the system is always finite but continually changing, we can explore a potentially infinite phase space which would otherwise be inaccessible with finite computer resources. Third, the enlarged capacity of systems with meta-dynamics for variation allows us to conduct true evolution experiments. The modeling methods presented here can be applied to many real biological systems. In the two studies we present, we are investigating two apparent properties of adaptive networks. With the simulation of the prebiotic soup, we are most interested in how a chemical reaction network might emerge from an initial state of relative disorder. With the study of the immune system, we study the self-regulation of the network including its ability to distinguish between species which are part of the network and those which are not.
Adaptation, Biological↗