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Play in evolution, culture, and individual adaptation: implications for therapy.

In this paper human play is examined from the perspective of its role in evolution. A model of social evolution is proposed to extend the model of biological evolution and to demonstrate the central role of play in the social-evolutionary process. Since in evolution play is a mechanism for its process, it demands species members who are playful. Thus, man is a player by virtue of species membership and the evolutionary pathway of the species. The implications of this deep-seated characteristic of playfulness are discussed in terms of human development. Finally, a set of principles is derived from the evolutionary-developmental characteristics of play. Application of these principles in clinical practice is demonstrated and discussed.

Adolescent

A kin selection model for the evolution of virulence.

The costs and benefits of parasite virulence are analysed in an evolutionarily stable strategy (ESS) model. Increased host mortality caused by disease (virulence) reduces a parasite's fitness by damaging its food supply. The fitness costs of high virulence may be offset by the benefits of increased transmission or ability to withstand the host's defences. It has been suggested that multiple infections lead to higher virulence because of competition among parasite strains within a host. A quantitative prediction is given for the ESS virulence rate as a function of the coefficient of relatedness among co-infecting strains. The prediction depends on the quantitative relation between the costs of virulence and the benefits of transmission or avoidance of host defences. The particular mechanisms by which parasites can increase their transmission or avoid host defences also have a key role in the evolution of virulence when there are multiple infections.

Animals

A model for the evolution of networks of genes.

An organism persists through the activity of structural genes, which is co-ordinated by clusters of coupled regulatory genes. During evolution, changes of coupling within a cluster can increase the reliability with which its structural genes perform a task. To study the evolution of coupling, we have simulated and analyzed a stochastic model for a simple problem. The assumptions of the model are these: A network of regulatory genes co-ordinates the synthesis of four structural proteins, which associate in distinct heterodimers that form a heterotetramer. Mutation in cis-regulatory regions produces transitions among 64 types of network. In a population, each network reproduces in proportion to its fitness, which depends on its probability (reliability) of synthesizing the tetramer. Fitness-dependent attrition keeps the size of the population constant. Regulatory genes occur in a sequence of levels; each level is associated with a different family of transcription factors. The following results emerge: Because different messengers within a family can give networks with the same connectivity, the 64 types of networks cluster into eight equivalence classes. During evolution with a low mutation rate, high-fitness classes can be approached through various paths on a fitness landscape. With a higher mutation rate, networks remain more uniformly distributed among the 64 types, and lower-fitness networks remain preponderant. An initially homogeneous population becomes more heterogeneous through mutation, but selection according to fitness later reduces its diversity. During this process the dispersion of the population over the possible networks increases, then decreases as the population approaches a unique steady state.

Animals

A model for the evolution of reproductive skew without reproductive suppression

Reproductive skew is a measure of the way breeding is distributed among the members of an animal society or group. Up to now, explanations of patterns of skew have been limited to one particular model, which assumes that a single dominant has full control over the distribution of subordinate reproduction. If this control is incomplete or absent, however, unsanctioned breeding by subordinate females will increase the total number of young produced. Here I present a new model for the evolution of skew that considers the effect of brood size on the inclusive fitness of dominants and subordinates. By augmenting brood size, a subordinate female reduces the per capita fitness of a dominant's offspring, so the net benefits of producing young are lower for related subordinates. I consider the stable level of skew when both dominant and subordinate attempt to maximize their inclusive fitness under two conditions: (1) when the dominant is unable to anticipate that a subordinate will add to her brood; and (2) the dominant does anticipate subordinate reproduction and can respond by adjusting her own brood size. In the first case, the model predicts that reproductive skew will increase with relatedness between breeders, because related subordinates are selected to add fewer young to the dominant's brood. In the second case, the dominant's optimal response to the presence of a second breeder exaggerates the relationship between relatedness and skew: dominants should produce more young when breeding with related compared with unrelated subordinates. Copyright 1998 The Association for the Study of Animal Behaviour.

Journal Article

Cloning of the HSP70 gene from Halobacterium marismortui: relatedness of archaebacterial HSP70 to its eubacterial homologs and a model for the evolution of the HSP70 gene.

Heat shock induces the synthesis of a set of proteins in Halobacterium marismortui whose molecular sizes correspond to the known major heat shock proteins. By using the polymerase chain reaction and degenerate oligonucleotide primers for conserved regions of the 70-kDa heat shock protein (HSP70) family, we have successfully cloned and sequenced a gene fragment containing the entire coding sequence for HSP70 from H. marismortui. HSP70 from H. marismortui shows between 44 and 47% amino acid identity with various eukaryotic HSP70s and between 51 and 58% identity with its eubacterial and archaebacterial homologs. On the basis of a comparison of all available HSP70 sequences, we have identified a number of unique sequence signatures in this protein family that provide a clear distinction between eukaryotic organisms and prokaryotic organisms (archaebacteria and eubacteria). The archaebacterial (viz., H. marismortui and Methanosarcina mazei) HSP70s have been found to contain all of the signature sequences characteristic of eubacteria (particularly the gram-positive bacteria), which suggests a close evolutionary relationship between these groups. In addition, detailed analyses of HSP70 sequences that we have carried out have revealed a number of additional novel features of the HSP70 protein family. These include (i) the presence of an insertion of about 25 to 27 amino acids in the N-terminal quadrants of all known eukaryotic and prokaryotic HSP70s except those from archaebacteria and the gram-positive group of bacteria, (ii) significant sequence similarity in HSP70 regions comprising its first and second quadrants from organisms lacking the above insertion, (iii) highly significant similarity between a protein, MreB, of Escherichia coli and the N-terminal half of HSP70s, (iv) significant sequence similarity between the N-terminal quadrant of HSP70 (from gram-positive bacteria and archaebacteria) and the m-type thioredoxin of plant chloroplasts. To account for these and other observations, a model for the evolution of HSP70 proteins involving gene duplication is proposed. The model proposes that HSP70 from archaebacteria (H. marismortui and M. mazei) and the gram-positive group of bacteria constitutes the ancestral form of the protein and that all other HSP70s (viz., other eubacteria as well as eukaryotes) containing the insert have evolved from this ancient protein.

Amino Acid Sequence

Genetic variation in the Heterodoxus octoseriatus group (Phthiraptera): a test of Price's model of parasite evolution.

Most of the genetic variation in the H. octoseriatus group is present as fixed gene differences between species which have been described on morphological criteria. Based on allozymes, the taxonomic status of some species was challenged. There was insufficient evidence, however, to demonstrate that these were not 'good' biological species. Overall, the limited intraspecific variation was present as fixed gene differences among lice from different hosts and from different colonies of hosts; heterozygotes were rare. Two predictions derived from Price's model of parasite evolution were met: populations of lice were genetically homogeneous and, where genetic markers were present, we found substantial genetic variation among populations. These data contrast with those for endoparasitic helminths, where, in general, the amount of genetic variation is similar to that of free-living invertebrates.

Animals

[Modelling of spatial evolution and dynamics of a population of healthy then rabies infected foxes].

The authors describe the main feature of a computer model which helps to simulate the evolution of a rabies epi-enzootic in foxes. They show first the goals and interests of the study, then the originality of used methodology. Their results deal successively with dynamic evolution of a healthy population of foxes, then with this same population infected with rabies and, at last, spatial and temporal evolution of the enzootics. Simulated results are discussed by comparison with those observed in the field.

Animals

Functional morphology of beta cells in the area centralis of the cat's retina: a model for the evolution of central retinal specializations.

The dendritic morphology of beta cells in and around the area centralis of the retinae of normally pigmented and Siamese cats is described. Individual central beta cells in the Siamese cat do not differ morphologically from central beta cells in normally pigmented cats, and in both groups of animals, there is a clear morphological continuity between central and peripheral beta cells. On the basis of systematic patterns of beta cell dendritic orientation, ther area centralis of the normal cat can be divided into a central region, approximately 200 micrometers in diameter, and a pericentral region, approximately 1,400 micrometers in diameter. In the central region, nearly all beta cells have a single large primary dendrite which descends perpendicular to the plane of inner plexiform layer, and gives rise to a dendritic tree which is vertically aligned with the cell's soma. In the pericentral region, the single primary dendrite of most cells descends obliquely through the inner plexiform layer and gives rise to a dendritic tree which is displaced laterally from the position of the soma. For most of the cells the trajectory of the dendrite is systematically related to the location of the cell relative to the area centralis such that the somas are displaced away from its center, presumably in order to minimize the thickness of the ganglion cell layer in the high acuity region. Many beta cells outside the pericentral region also have oriented single primary dendrites, but their orientation seems fairly random with respect to the location of the area centralis. In the Siamese area centralis, this systematic pattern of beta cell dendritic orientation is markedly reduced, suggesting that the pattern is under genetic control. On the basis of these observations, a model for the evolution of the area centralis and fovea is presented which involves selection for systematic for systematic patterns of dendritic orientation in regions of high ganglion cell density.

Animals

A model for the evolution of the plastid sec apparatus inferred from secY gene phylogeny.

Plastids possess a bacteria-like sec apparatus that is involved in protein import into the thylakoid lumen. We have analyzed one of the genes essential for this process, secY. A secY gene from the unicellular red alga Cyanidium caldarium was found to be transcriptionally active, demonstrating for the first time that secY is functional in a plastid. Unlike the situation seen in bacteria the C. caldarium gene is transcribed monocistronically, despite the fact that it is part of a large ribosomal gene cluster that resembles bacterial spc operons. A molecular phylogeny is presented for 8 plastid-encoded secY genes, four of which have not been published yet. In this analysis plastid secY genes fall into two classes. One of these, comprising of genes from multicellular red algae and Cryptophyta, clusters in a neighbour-joining tree with a cyanobacterial counterpart. Separated from the aforesaid are secY genes from Chromophyta, Glaucocystophyta and a unicellular red alga. All plastid and cyanobacterial sequences are located on the same branch, separated from bacterial homologues. We postulate that the two classes of secY genes are paralogous, i.e. their gene products are involved in different protein translocation processes. Based on this assumption a model for the evolution of the plastid sec apparatus is presented.

Cloning, Molecular

Genetic and strategic models for the evolution of mating systems.

Male and female fitnesses in the Shaw-Mohler equation are partitioned into components which putatively determine mating systems. The resultant genetic models provide criteria for evolutionary stable population states and yield strategic models based on maximization principles and fitness sets.

Alleles

A domain model for eukaryotic DNA organization: a molecular basis for cell differentiation and chromosome evolution.

A model for eukaryotic chromatin organization is presented in which the basic structural and functional unit is the DNA domain. This simple model predicts that both chromosome replication and cell type-specific control of gene expression depend on a combination of stable and dynamic DNA-nuclear matrix interactions. The model suggests that in eukaryotes, DNA regulatory processes are controlled mainly by the intranuclear compartmentalization of the specific DNA sequences, and that control of gene expression involves multiple steps of specific DNA-nuclear matrix interactions. Predictions of the model are tested using available biochemical, molecular and cell biological data. In addition, the domain model is discussed as a simple molecular mechanism to explain cell differentiation in multi-cellular organisms and to explain the evolution of eukaryotic genomes consisting mainly of repetitive sequences and "junk" DNA.

Animals

A mathematical model of biological evolution.

In order to understand generally how the biological evolution rate depends on relevant parameters such as mutation rate, intensity of selection pressure and its persistence time, the following mathematical model is proposed: dNn(t)/dt = (mn(t) - mu)Nn(t) + muNn-1(t) (n = 0,1,2,3,...), where Nn(t) and mn(t) are respectively the number and Malthusian parameter of replicons with step number n in a population at time t and mean is the mutation rate, assumed to be a positive constant. The step number of each replicon is defined as either equal to or larger by one than that of its parent, the latter case occurring when and only when mutation has taken place. The average evolution rate defined by v infinity identical to lim t leads to infinity sigma infinity n = o nNn(t)/t sigma infinity n = o Nn(t) is rigorously obtained for the case (i) mn(t) = mn is independent of t (constant fitness model), where mn is essentially periodic with respect to n, and for the case (ii) mn(t) = s(-1) n+[t/tau] (periodic fitness model), together with the long time average -m infinity of the average Malthusian parameter -m identical to sigma infinity n = o mn(t)Nn(t)/sigma infinity n = o Nn(t). The biological meaning of the results is discussed, comparing them with the features of actual molecular evolution and with some results of computer simulation of the model for finite populations.

Animals

Non random DNA evolution.

A model for testing random molecular evolution is proposed. Randomness of recurrent mutation is defined based on isotropy and zero covariance among nucleotide sites. Assuming an equal rate of mutation for the bases A, T, G, and C, in both DNA strands, a mutational matrix of transformation A, T, G, and C with 6 parameters is developed. Under this model the equilibrium proportions (F) of the bases are FA = FT = (D + E)/[2(D + E + H + J)] and FG = FC = (H + J)/[2(D + E + H + J)], D, E, H, J being 4 of the 6 matrix parameters. Thus the expected (FA + FT)/(FG + FC) ratio can also be tested. If the average rate of mutation is 10(-8) per nucleotide site and cell replication, the equilibrium for every site, in most species, is reached in 10(8) years. Eight DNA segments from human, bacteria, fungus and insect genomes were chosen to test these proportions and their heterogeneity among coding and non coding subsegments. While FG was similar to FC as expected, FA was highly different from FT Huge heterogeneities were found between coding and non coding segments and among non coding segments. These results are a strong evidence for non randomness of molecular evolution.

Animals

[Tandem DNA repeats in the vertebrate genome: structure, possible mechanisms of formation and evolution].

Possible models for the generation and the evolution of tandem repeats are discussed. The model of A.J. Jeffreys and co-workers as well as facts, supporting or contradicting this model are discussed. Facts supporting the hypothesis of the generation of the tandem repeats as the result of mitotic recombination are described. On the basis of an analysis of the structure of the tandem repeats containing loci, it is supposed that there exist space and time relations between the multimerization of the tandem repeats and tandem gene duplication. On the basis of this supposition, the generation of majority of the tandem repeated gene as a result of sister chromatids recombination in mitosis is proposed. Factors determining the existence of recombination hotspots of are discussed. Some specific features of the evolution of tandem repeats of the coding region are also described.

Animals