No abstract

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. We demonstrate that reactions differ significantly in their relative impact on the total noise and we illustrate the importance of protein degradation on the overall variability for a range of molecular processes and signaling systems. With our flexible and generally applicable noise decomposition method, we are able to shed new, to our knowledge, light on the sources and propagation of noise in biochemical reaction networks; in particular, we are able to show how regulated protein degradation can be employed to reduce the noise in biochemical systems.

We provide a classification of symmetric three-player games with two strategies and investigate evolutionary and asymptotic stability (in the replicator dynamics) of their Nash equilibria. We discuss similarities and differences between two-player and multi-player games. In particular, we construct examples which exhibit a novel behavior not found in two-player games. Copyright Springer-Verlag 2004multi-player games, evolutionarily stable strategies, asymptotic stability, replicator dynamics, risk-dominance,

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.We propose a new methodology to deal with time delays in biological systems and apply it to simple models of gene expression with delayed degradation. We show that time delay of protein degradation does not cause oscillations as it was recently argued. It follows from our rigorous analysis that one should look for different mechanisms responsible for oscillations observed in biological experiments.We develop a systematic analytical treatment of stochastic models of time delays. Specifically we take into account that some reactions, for example degradation, are consuming, that is: once molecules start to degrade they cannot be part in other degradation processes. We introduce an auxiliary stochastic process and calculate analytically the variance and the autocorrelation function of the number of protein molecules in stationary states in basic models of delayed protein degradation.

We extend the classical Barabási-Albert preferential attachment procedure to graphs with internal vertex structure given by weights of vertices. In our model, weight dynamics depends on the current vertex degree distribution and the preferential attachment procedure takes into account both weights and degrees of vertices. We prove that such a coupled dynamics leads to scale-free graphs with exponents depending on parameters of the weight dynamics.