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At least 235 records · Page 13Linked to original sources
PubMed1986

Natural selection, fitness entropy, and the dynamics of coevolution.

The coevolutionary dynamics of interacting populations were studied by combining continuous time Lotka-Volterra models of population growth with single-locus genetic models of weak selection. The effects of natural selection on population growth were evaluated using Ginzburg's fitness entropy function as a measure of the deviation of a population's initial allele frequencies from their polymorphic equilibrium values. This entropy measure was used to relate the dynamics of a community composed of evolving populations to the dynamics of a "reference community" whose populations are initially in genetic equilibrium. Specifically, a quantity called the "selective difference area" was defined as the total difference between the population size trajectories of a reference and evolving population. The selective difference area represents the amount of extra life a species would realize if the entire community were at genetic equilibrium. It was shown that this selective difference area is a simple linear function of the initial fitness entropies of each species. This prediction is independent of the strength of selection and holds for any arbitrary set of initial population densities. Numerical examples were presented to illustrate the results. Under the assumption of weak selection, a generalization for arbitrary population growth models was outlined.

Biological Evolution↗
PubMed1991

Coevolution of self-fertilization and inbreeding depression. I. Mutation-selection balance at one and two loci.

Simple theories for the evolution of breeding systems suggest that the fate of an allele that modifies the rate of self-fertilization hinges only on the degree to which selfing reduces opportunities for outcrossing ("pollen discounting") and the extent of inbreeding depression. These theories predict that outcrossing evolves whenever deleterious mutations have a more severe effect in combination than expected from their individual effects. We study the evolutionary dynamics of a modifier of the rate of self-fertilization in populations subject to complete pollen discounting and recurrent mutations which impair viability at a single locus in diploids and at two loci in haploids. Our analysis indicates that genetic associations arising immediately upon the introduction of a rare modifier allele generate substantial quantitative and qualitative departures from expectation. Higher rates of segregation under selfing in our one-locus diploid model generate positive associations between enhancers of selfing and wild-type viability alleles, which in turn favor the evolution of selfing under a wider range of conditions than expected. Greater opportunities for recombination under outcrossing in our two-locus haploid model generate positive associations between enhancers of outcrossing and wild-type viability alleles. These associations favor the evolution of outcrossing under a wider range of conditions, and introduce the possibility of stable mixed mating systems involving both selfing and outcrossing. Our explicit analysis of genetic associations between loci affecting viability and the rate of self-fertilization indicates that modifiers that enhance the production of offspring with very high (and very low) viability by promoting segregation or recombination develop positive associations with high viability. This advantage of producing extremes can compensate for an initial disadvantage in offspring number.

Alleles↗
PubMed1991

Coevolution of self-fertilization and inbreeding depression. III. Homozygous lethal mutations at multiple loci.

We study the evolution of the rate of self-fertilization in response to deleterious mutations at multiple loci. Although partial selfing induces associations among loci even in the absence of linkage, associations among mutations at different loci are of a smaller order of magnitude than the mutation rate. Genotypes that carry homozygous lethal mutations in heterozygous form at i loci occur in frequencies of the order (Ti) mu i, in which T denotes the number of viability loci and mu the mutation rate. While associations between mutations at different loci remain small even under inbreeding, each viability locus develops an association with the modifier of the rate of self-fertilization that substantially affects the evolution of the breeding system. Positive associations between enhancers of selfing and haplotypes carrying multiple wild-type alleles and positive associations in heterozygosity between the modifier locus and the viability loci promote evolutionary increases in the rate of self-fertilization.

Biometry↗
PubMed1992

Coevolution of cytokine receptor families in the immune and nervous systems.

Close relationships between the nervous system and immune systems at molecular levels have now become evident. Receptors for CDF/LIF and CNTF, i.e., factors which play important roles in the nervous system, share a close structural similarity to those for IL-6, which is a molecule acting in the immune system. Receptors for these three factors belong to a subtype of cytokine receptor family (class IB cytokine receptor). We have constructed a higher subdomain structure of the receptor for CDF/LIF based on its known primary structures. The receptor contains immunoglobulin and fibronectin-like domains, in addition to common domains of the cytokine receptor, similar to those cell surface molecules of the neural immunoglobulin gene super family. These domains appear to have similar structures to the immunoglobulin. These lines of evidence suggest that the class IB cytokine receptor was formed as a result of those fusion of the genes for a more primitive cytokine receptor IA and for the neural immunoglobulin super gene family, and that, likewise, many molecules regulating neural development and those which act in the immune system have a common evolutionary origin.

Amino Acid Sequence↗
PubMed1984

Coevolution of functionally constrained characters: prerequisites for adaptive versatility.

One of the major problems of organismic evolution theory is to explain how complex organisms were able to evolve by random mutations in spite of the severe functional constraints that canalize their route of change. The problem is discussed on the basis of a quantitative genetic model. How the degree of genetic variation influences the adaptation speed of functionally coupled but genetically uncorrelated characters is examined. It was found, that if more than three independent characters contribute to the variation of a functionally constrained system, optimal degrees of genetic variation exist. Higher degrees of variation lead to decreasing adaptation rates. Conversely, functional constraints do not limit the degree of adaptely reasonable genetic variability as long as the number of independent characters is not higher than three. The conclusion is drawn that there is no need to develop a genetic correlation between functionally coupled characters as long as not many more than three characters are integrated into a functional system. This explains the fact that there is no genetic coupling between the inherited signal sender and receiver mechanisms in orthopterians, even though there is a strong functional coupling between them.

Adaptation, Biological↗
PubMed1994

Coevolution of papillomaviruses with human populations.

The human papillomavirus types that are causally linked to genital cancer originated in ancient times in prehuman primates. The molecular diversity of viral isolates reflects the African origins and the subsequent worldwide spread of human races. The lack of transmission of papillomaviruses between species may support a gradual mode of molecular evolution.

Biological Evolution↗
PubMed2005

Coevolution of cancer and stromal cellular responses.

It is now becoming apparent that multiple types of stromal cells, including macrophages, mast cells, adipocytes, and fibroblasts make pivotal contributions to carcinogenesis. In the May 6 issue of Cell, Orimo and colleagues (Orimo et al., 2005) show that carcinoma-associated fibroblasts can promote epithelial tumorigenesis by secreting the chemokine SDF-1alpha (CXCL12). SDF-1alpha stimulates carcinoma cell proliferation and recruitment of endothelial precursor cells.

Animals↗
PubMed2005

Coevolution of protein and RNA structures within a highly conserved ribosomal domain.

The X-ray crystal structure of a ribosomal L11-rRNA complex with chloroplast-like mutations in both protein and rRNA is presented. The global structure is almost identical to that of the wild-type (bacterial) complex, with only a small movement of the protein alpha helix away from the surface of the RNA required to accommodate the altered protein residue. In contrast, the specific hydrogen bonding pattern of the mutated residues is substantially different, and now includes a direct interaction between the protein side chain and an RNA base edge and a water-mediated contact. Comparison of the two structures allows the observations of sequence variation and relative affinities of wild-type and mutant complexes to be clearly rationalized, but reinforces the concept that there is no single simple code for protein-RNA recognition.

Base Sequence↗
PubMed2006

Coevolution of exceptional longevity, exceptionally high metabolic rates, and mitochondrial DNA-coded proteins in mammals.

Mammals' longevity is inversely related to mass-specific basal metabolic rate because the generation of reactive oxygen species constrains lifespan. Longevity increases with body mass because the latter is inversely related to mass-specific basal metabolic rates. In placental mammals the longevity residuals from the power laws that describe longevity as a function of mass-specific basal metabolic rates, or body mass, are positively correlated with the relative rates of evolution of cytochrome b, a generator of reactive oxygen species. Therefore, longevity is more accurately described as a function of both mass-specific basal metabolic rate and the relative rate of cytochrome b evolution. The longevity residuals from the power law that describe longevity as a function of body mass are positively correlated with the relative rate of evolution of most other mtDNA-coded proteins. In taxa with very high rate of cytochrome b evolution exceptional longevity is associated with an increase, rather than the predicted decrease, of basal metabolic rates. These finding are compatible with the hypothesis that, in placental mammals, the accelerated evolution of mtDNA-coded proteins, allowed the extension of lifespan by selecting mutations that reduce the generation of reactive oxygen species, mostly by increasing internal proton leak, that accelerates mitochondrial electron transport.

Adaptation, Physiological↗
PubMed2005

Elucidation of subfamily segregation and intramolecular coevolution of the olfactomedin-like proteins by comprehensive phylogenetic analysis and gene expression pattern assessment.

The categorization of genes by structural distinctions relevant to biological characteristics is very important for understanding of gene functions and predicting functional implications of uncharacterized genes. It was absolutely necessary to deploy an effective and efficient strategy to deal with the complexity of the large olfactomedin-like (OLF) gene family sharing sequence similarity but playing diversified roles in many important biological processes, as the simple highest-hit homology analysis gave incomprehensive results and led to inappropriate annotation for some uncharacterized OLF members. In light of evolutionary information that may facilitate the classification of the OLF family and proper association of novel OLF genes with characterized homologs, we performed phylogenetic analysis on all 116 OLF proteins currently available, including two novel members cloned by our group. The OLF family segregated into seven subfamilies and members with similar domain compositions or functional properties all fell into relevant subfamilies. Furthermore, our Northern blot analysis and previous studies revealed that the typical human OLF members in each subfamily exhibited tissue-specific expression patterns, which in turn supported the segregation of the OLF subfamilies with functional divergence. Interestingly, the phylogenetic tree topology for the OLF domains alone was almost identical with that of the full-length tree representing the unique phylogenetic feature of full-length OLF proteins and their particular domain compositions. Moreover, each of the major functional domains of OLF proteins kept the same phylogenetic feature in defining similar topology of the tree. It indicates that the OLF domain and the various domains in flanking non-OLF regions have coevolved and are likely to be functionally interdependent. Expanded by a plausible gene duplication and domain couplings scenario, the OLF family comprises seven evolutionarily and functionally distinct subfamilies, in which each member shares similar structural and functional characteristics including the composition of coevolved and interdependent domains. The phylogenetically classified and preliminarily assessed subfamily framework may greatly facilitate the studying on the OLF proteins. Furthermore, it also demonstrated a feasible and reliable strategy to categorize novel genes and predict the functional implications of uncharacterized proteins based on the comprehensive phylogenetic classification of the subfamilies and their relevance to preliminary functional characteristics.

Amino Acid Sequence↗
PubMed2005

Rapid expansion of killer cell immunoglobulin-like receptor genes in primates and their coevolution with MHC Class I genes.

The gene family of killer cell immunoglobulin-like receptors (KIRs) in primates provides the first line of defense against virus infection and tumor transformation. Interacting with MHC class I molecules, KIRs can regulate the cytotoxic activity of natural killer (NK) cells and distinguish the tumor and virus infected cells from normal body cells. Phylogenetic analysis and comparison of domain structures identified three major groups of KIR genes (group I, II, and III genes). These groups of KIR genes, generated by a series of gene duplications, have acquired different MHC-binding specificity. Inference of ancestral KIR sequences suggested that the functional divergence of group I genes from group II genes occurred by positive selection at the MHC-binding sites after duplication. Our evolutionary study has shown that group I genes diverged from group II genes about 17 million years ago (Mya) apparently after separation of hominoids from Old World (OW) monkeys. Around the same time, gene duplication generating the class I MHC-C locus appears to have occurred. These findings suggest that KIR and MHC class I genes have coevolved as an interacting system. The KIR gene family has experienced a rapid expansion in primate species. The rate of expansion of this gene family seems to be one of the highest among all hominoid gene families. The KIR gene family is also subject to birth-and-death evolution.

Amino Acid Sequence↗
PubMed2005

On the coevolution of genes and genetic code.

The canonical genetic code acts efficiently in minimizing the effects of mistranslations and point mutations. In the work presented we have also considered the effects of single nucleotide insertions and deletions on the optimality of the genetic code. Our results suggest that the canonical genetic code compensates for the ins/del mutations as well as mistranslations and point mutations. On the other hand, we highlighted the point that ins/del mutations have a lesser impact on the selected genes of Saccharomyces cerevisiae compared to randomly generated ones. We hypothesized that the codon usage preferences in S. cerevisiae genes are responsible for the higher efficiency of translation machinery in this organism. Our results support the conjecture that codon usage preferences render the genetic code more effective in minimizing the effects of ins/del mutations.

Animals↗
PubMed2006

Early coevolution of adhesive but not antiadhesive tenascin-R ligand-receptor pairs in vertebrates: a phylogenetic study.

Axon growth inhibitory CNS matrix proteins, such as tenascin-R (TN-R), have been supposed to contribute to the poor regenerative capacity of adult mammalian CNS. With regard to TN-R function in low vertebrates capable of CNS regeneration, questions of particular interest concern the (co)evolution of ligand-receptor pairs and cellular response mechanisms associated with axon growth inhibition and oligodendrocyte differentiation. We address here these questions in a series of comparative in vivo and in vitro analyses using TN-R proteins purified from different vertebrates (from fish to human). Our studies provide strong evidence that unlike TN-R of higher vertebrates, fish TN-R proteins are not repellent for fish and less repellent for mammalian neurons and do not interfere with F3/contactin- and fibronectin-mediated mammalian cell adhesion and axon growth. However, axonal repulsion is induced in fish neurons by mammalian TN-R proteins, suggesting that the intracellular inhibitory machinery induced by TN-R-F3 interactions is already present during early vertebrate evolution. In contrast to TN-R-F3, TN-R-sulfatide interactions, mediating oligodendrocyte adhesion and differentiation, are highly conserved during vertebrate evolution. Our findings thus indicate the necessity of being cautious about extrapolations of the function of ligand-receptor pairs beyond a species border and, therefore, about the phylogenetic conservation of a molecular function at the cellular/tissue level.

Animals↗
PubMed2005

Modelling brain emergent behaviours through coevolution of neural agents.

Recently, many research efforts focus on modelling partial brain areas with the long-term goal to support cognitive abilities of artificial organisms. Existing models usually suffer from heterogeneity, which constitutes their integration very difficult. The present work introduces a computational framework to address brain modelling tasks, emphasizing on the integrative performance of substructures. Moreover, implemented models are embedded in a robotic platform to support its behavioural capabilities. We follow an agent-based approach in the design of substructures to support the autonomy of partial brain structures. Agents are formulated to allow the emergence of a desired behaviour after a certain amount of interaction with the environment. An appropriate collaborative coevolutionary algorithm, able to emphasize both the speciality of brain areas and their cooperative performance, is employed to support design specification of agent structures. The effectiveness of the proposed approach is illustrated through the implementation of computational models for motor cortex and hippocampus, which are successfully tested on a simulated mobile robot.

Animals↗