Biomedical subjects

N Behera

Publications and source records attributed to N Behera.

4 recordsLinked to original sources

PubMed1997

Trans gene regulation in adaptive evolution: a genetic algorithm model.

This is a continuation of earlier studies on the evolution of infinite populations of haploid genotypes within a genetic algorithm framework. We had previously explored the evolutionary consequences of the existence of indeterminate-"plastic"-loci, where a plastic locus had a finite probability in each generation of functioning (being switched "on") or not functioning (being switched "off"). The relative probabilities of the two outcomes were assigned on a stochastic basis. The present paper examines what happens when the transition probabilities are biased by the presence of regulatory genes. We find that under certain conditions regulatory genes can improve the adaptation of the population and speed up the rate of evolution (on occasion at the cost of lowering the degree of adaptation). Also, the existence of regulatory loci potentiates selection in favour of plasticity. There is a synergistic effect of regulatory genes on plastic alleles: the frequency of such alleles increases when regulatory loci are present. Thus, phenotypic selection alone can be a potentiating factor in a favour of better adaptation.

Adaptation, Physiological↗

PubMed1996

The consequences of phenotypic plasticity in cyclically varying environments: a genetic algorithm study.

By "phenotypic plasticity" we refer to the capacity of a genotype to exhibit different phenotypes, whether in the same or in different environments. We have previously demonstrated that phenotypic plasticity can improve the degree of adaptation achieved via natural selection (Behera & Nanjundiah, 1995). That result was obtained from a genetic algorithm model of haploid genotypes (idealized as one-dimensional strings of genes) evolving in a fixed environment. Here, the dynamics of evolution is examined under conditions of a cyclically varying environment. We find that the rate of evolution, as well as the extent of adaptation (as measured by mean population fitness) is lowered because of environmental cycling. The decrease in adaptation caused by a varying environment can, however, be partly or wholly compensated by an increase in the degree of plasticity that a genotype is capable of. Also, the reduction of population fitness caused by a variable environment can be partially offset by decreasing the total number of genetic loci. We conjecture that an increase in genome size may have been among the factors responsible for the evolution of phenotypic plasticity.

Adaptation, Physiological↗

PubMed1996

Variational principles in evolution.

For a one-locus selection model, Svirezhev introduced an integral variational principle by defining a Lagrangian which remained stationary on the trajectory followed by the population undergoing selection. It is shown here (i) that this principle can be extended to multiple loci in some simple cases and (ii) that the Lagrangian is defined by a straightforward generalization of the one-locus case, but (iii) that in two-locus or more general models there is no straightforward extension of this principle if linkage and epistasis are present. The population trajectories can be constructed as trajectories of steepest ascent in a Riemannian metric space. A general method is formulated to find the metric tensor and the surface in the metric space on which the trajectories, which characterize the variations in the gene structure of the population, lie. The local optimality principle holds good in such a space. In the special case when all possible linkage disequilibria are zero, the phase point of the n-locus genetic system moves on the surface of the product space of n higher dimensional unit spheres in a certain Riemannian metric space of gene frequencies so that the rate of change of mean fitness is maximum along the trajectory. In the two-locus case the corresponding surface is a hyper-torus.

Biological Evolution↗

PubMed1995

An investigation into the role of phenotypic plasticity in evolution.

Phenotypic plasticity can modify evolutionary pathways and accelerate the course of evolution. This was brought out in a quantitative model by Hinton & Nowlan (1987, Complex Systems 1, 497-502). The present work confirms and extends their results. We consider a population of genetically haploid individuals of fixed size. Genotypes are represented by one-dimensional arrays (strings) of genes. Each gene can be in one of three allelic states, designated 1, 0 and X. 1 and 0 stand for fixed states, that is for states with predetermined effects on the phenotype. X stands for a plastic state: the phenotypic effect of an X can be equivalent to that of a 1 or a 0, the actual choice being realized by a process of random coin-tossing. Our model, in contrast to that of Hinton and Nowlan, assumes a relatively smooth dependence of fitness on distance from a pre-assigned target genotype. From the fitness values, the number of individuals reaching reproductive maturity is determined. Reproduction involves random mating and a single recombinational event, with one of the two progeny genotypes becoming, in turn, a possible parental genotype for the next generation. We find that it is because of the special assumptions in the Hinton and Nowlan model that phenotypic plasticity invariably accelerates evolution. The relationship is not as straightforward with realistic fitness schemes. Instead, the general result is that plasticity, up to a certain optimal level, slows down the rate of evolutionary change but improves the level of adaptation finally reached.

Adaptation, Physiological↗