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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.
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.
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.
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.
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The notion of an evolutive hierarchical system proposed here retains the following characteristics of some natural systems, like living organisms: they have an internal organization consisting of more or less complex components with interrelations; they maintain their organization in time although their components are changing; they may be studied at several complexity levels (e.g., molecular, cellular, ...). The idea is to model the state of the system at a given instant by a category, the state transition by a functor, a complex object by the (direct) limit of a pattern of linked objects (its own organization). The emergence of new properties for a complex object is measured, and a development process is described.
A population genetic approach is presented for general analysis and comparison of kin selection models of sib and half-sib altruism. Nine models are described, each assuming a particular mode of inheritance, number of female inseminations, and Mendelian dominance of the altruist gene. In each model, the selective effects of altruism are described in terms of two general fitness functions, A(beta) and S(beta), giving respectively the expected fitness of an altruist and a nonaltruist as a function of the fraction of altruists beta in a given sibship. For each model, exact conditions are reported for stability at altruist and nonaltruist fixation. Under the Table 3 axions, the stability conditions may then be partially ordered on the basis of implications holding between pairs of conditions. The partial orderings are compared with predictions of the kin selection theory of Hamilton.
A model for eukaryotic DNA organization has been proposed in which DNA regulatory processes depend on multiple site-specific DNA-nuclear matrix interactions throughout a DNA domain. In this model gene regulation depends on combinations of a few control factors in a cell to activate cell type-specific genes. This model suggests simple molecular mechanisms for organismal development which can account for sequential activation of appropriate groups of genes throughout development and for specific constraints on developmental pathways. Additionally, these suggested developmental pathways are consistent with mechanisms of evolution in which gradualism and punctuated equilibrium are not exclusive of one another and are interrelated mechanisms of evolution that are both induced by specific chromosomal mutations.
Naturally occurring hemorrhagic and thrombotic diseases of animals closely parallel their human counterparts. While such models may be particularly useful in studying the pathogenesis of human disease, it is usually more realistic to depend upon experimentally induced disease models. The species selected for use is therefore of major importance in providing meaningful extrapolation to humans, as are the experimental design and type of procedure (in vitro, ex vivo, in vivo). Regardless of the test system used when in vitro procedures are employed, these must be translated eventually to the in vivo situation. Information about the normal aging process of different species is important here and should influence selection of the species and test system. The ideal situation may not be feasible or pertain because of cost, availability, size, and investigator familiarity, or lack thereof, with the most suitable species or model.
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Three patterns of DNA sequence conservation have been identified from five human and rodent genomic sequence comparisons. First, a divergent pattern was observed in the noncoding sequences of the beta-globin and gamma-crystallin gene clusters, and second, a highly conserved pattern was observed in the noncoding regions of the T cell receptor C alpha-C delta, and the alpha- and beta-myosin-heavy-chain genes. A third, mixed pattern has also been found in the immunoglobulin IgH C mu-C delta gene region. These three patterns of genomic evolution pose the fascinating possibility that large portions of the genome evolve at different rates.
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Nuclear lamins are intermediate filament (IF) type proteins that form a fibrillar network underlying the inner nuclear membrane. The existence of multiple subtypes of lamins in vertebrates has been interpreted in terms of functional specialization during cell division and differentiation. The structure of a gene encoding an A-type lamin of Xenopus laevis was analysed. Comparison with that of a B-type lamin of the same species shows remarkable conservation of the exon/intron pattern. In both genes the last exon, only 9-12 amino acids in length, encodes the complete information necessary for membrane targeting of lamins, i.e. a ras-related CaaX motif. The lamin A specific extension of the tail domain is encoded by a single additional exon. The 5' boundary of this exon coincides with the sequence divergence between human lamins A and C, for which an alternative splice mechanism had previously been suggested. Arguments are presented suggesting that B-type lamins represent the ancestral type of lamins and that A-type lamins derived there from by exon shuffling. The acquisition of the new exon might explain the different fates of A- and B-types lamins during cell division.
We examine a model evolutionary space consisting of genotypes mapped to their corresponding phenotypes. This mapping is derived from a lattice model for proteins which, despite its highly idealized nature, has been shown to share general properties with real proteins. Large evolutionary networks are observed, with genotypes corresponding to non-lethal phenotypes linked by unit mutational steps. Neutral mutations are necessary for traversing the evolutionary networks, and even one neutral mutation in a genotype can change the phenotypes attainable by a unit mutational step.
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In this paper the following problem is addressed: "Under what conditions can a collection of individual organisms learn to cooperate when cooperation appears to outwardly degrade individual performance at the outset. In order to attempt a theoretical solution to this problem, data from a real world problem in anthropology is used. A distributed simulation model of this system was developed to assess its long term behavior using using an approach suggested by Zeigler (Zeigler, B.P., 1984, Multifaceted Modelling and Discrete Event Simulation (Academic Press, London)). The results of the simulation are used to show that although cooperation degrades the performance potential of each individual, it enhances the persistence of the individual's partial solution to the problem in certain situations."