Publications by authors named "Jacek MieKisz"

Real-world processes often exhibit temporal separation between actions and reactions - a characteristic frequently ignored in many modelling frameworks. Adding temporal aspects, like time delays, introduces a higher complexity of problems and leads to models that are challenging to analyse and computationally expensive to solve. In this work, we propose an intermediate solution to resolve the issue in the framework of evolutionary game theory.

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We study effects of the mutant's degree on the fixation probability, extinction, and fixation times in Moran processes on Erdös-Rényi and Barabási-Albert graphs. We performed stochastic simulations and used mean-field-type approximations to obtain analytical formulas. We showed that the initial placement of a mutant has a significant impact on the fixation probability and extinction time, while it has no effect on the fixation time.

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It is usually expected that time delays cause oscillations in dynamical systems-there might appear cycles around stationary points. Here we study random walks with asymmetric time delays. In our models, the probability of a walker to move to the right or to the left depends on the difference between two state-dependent fitness functions evaluated at two different times.

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We study the effects of strategy-dependent time delays on the equilibria of evolving populations. It is well known that time delays may cause oscillations in dynamical systems. Here we report a novel behavior.

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The Letter presents a novel way to connect random walks, stochastic differential equations, and evolutionary game theory. We introduce a new concept of a potential function for discrete-space stochastic systems. It is based on a correspondence between one-dimensional stochastic differential equations and random walks, which may be exact not only in the continuous limit but also in finite-state spaces.

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Biological signals in cells are transmitted with the use of reaction cycles, such as the phosphorylation-dephosphorylation cycle, in which substrate is modified by antagonistic enzymes. An appreciable share of such reactions takes place in crowded environments of two-dimensional structures, such as plasma membrane or intracellular membranes, and is expected to be diffusion-controlled. In this work, starting from the microscopic bimolecular reaction rate constants and using estimates of the mean first-passage time for an enzyme-substrate encounter, we derive diffusion-dependent effective macroscopic reaction rate coefficients (EMRRC) for a generic reaction cycle.

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We investigate the kinetics of the ubiquitous phosphorylation-dephosphorylation cycle on biological membranes by means of kinetic Monte Carlo simulations on the triangular lattice. We establish the dependence of effective macroscopic reaction rate coefficients as well as the steady-state phosphorylated substrate fraction on the diffusion coefficient and concentrations of opposing enzymes: kinases and phosphatases. In the limits of zero and infinite diffusion, the numerical results agree with analytical predictions; these two limits give the lower and the upper bound for the macroscopic rate coefficients, respectively.

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In a recent paper [Phys. Rev. E 86, 011134 (2012)], Mobilia introduces cooperation facilitators in the standard prisoner's dilemma game.

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Stochasticity is an essential aspect of biochemical processes at the cellular level. We now know that living cells take advantage of stochasticity in some cases and counteract stochastic effects in others. Here we propose a method that allows us to calculate contributions of individual reactions to the total variability of a system's output.

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We analyze a simple model of a self-repressing system with multiple gene copies. Protein molecules may bound to DNA promoters and block their own transcription. We derive analytical expressions for the variance of the number of protein molecules in the stationary state in the self-consistent mean-field approximation.

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In many biochemical reactions occurring in living cells, number of various molecules might be low which results in significant stochastic fluctuations. In addition, most reactions are not instantaneous, there exist natural time delays in the evolution of cell states. It is a challenge to develop a systematic and rigorous treatment of stochastic dynamics with time delays and to investigate combined effects of stochasticity and delays in concrete models.

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Stochastic effects in gene expression may result in different physiological states of individual cells, with consequences for pathogen survival and artificial gene network design. We studied the contributions of a regulatory factor to gene expression noise in four basic mechanisms of negative gene expression control: 1), transcriptional regulation by a protein repressor, 2), translational repression by a protein; 3), transcriptional repression by RNA; and 4), RNA interference with the translation. We investigated a general model of a two-gene network, using the chemical master equation and a moment generating function approach.

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Animal behavior and evolution can often be described by game-theoretic models. Although in many situations the number of players is very large, their strategic interactions are usually decomposed into a sum of two-player games. Only recently were evolutionarily stable strategies defined for multi-player games and their properties analyzed [Broom, M.

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We propose a game-theoretic dynamics of a population of replicating individuals. It consists of two parts: the standard replicator one and a migration between two different habitats. We consider symmetric two-player games with two evolutionarily stable strategies: the efficient one in which the population is in a state with a maximal payoff and the risk-dominant one where players are averse to risk.

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We discuss stochastic dynamics of populations of individuals playing games. Our models possess two evolutionarily stable strategies: an efficient one, where a population is in a state with the maximal payoff (fitness) and a risk-dominant one, where players are averse to risks. We assume that individuals play with randomly chosen opponents (they do not play against average strategies as in the standard replicator dynamics).

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We construct two models of discrete-time replicator dynamics with time delay. In the social-type model, players imitate opponents taking into account average payoffs of games played some units of time ago. In the biological-type model, new players are born from parents who played in the past.

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