Molecular networks guide the biochemistry of a living cell on multiple levels: its metabolic and signalling pathways are shaped by the network of interacting proteins, whose production, in turn, is controlled by the genetic regulatory network. To address topological properties of these two networks we quantify correlations between connectivities of interacting nodes and compare them to a null model of a network, in which al links were randomly rewired. We find that for both interaction and regulatory networks, links between highly connected proteins are systematically suppressed, while those between a highly-connected and low-connected pairs of proteins are favored. This effect decreases the likelihood of cross talk between different functional modules of the cell, and increases the overall robustness of a network by localizing effects of deleterious perturbations.With the growth of experimental information about basic biochemical mechanisms of life, molecular networks operating in living cells are becoming better defined. Direct physical interactions between pairs of proteins form one such network. It serves as a backbone for functional and structural relationships among its nodes and defines pathways for the propagation of various signals such as phosphorylation and allosteric regulation of proteins. The information about specific binding of proteins to each other has recently grown by an unprecedented amount as a result of high throughput two-hybrid experiments [1,2]. The production and degradation of proteins participating in the interaction network is controlled by the genetic regulatory network of the cell formed by all pairs of proteins in which the first protein directly regulates the abundance of the second. The majority of known cases of such regulation happens at the level of transcription, in which a transcription fac-1

No abstract

Chromosomal regions can adopt stable and heritable alternative states resulting in bistable gene expression without changes to the DNA sequence. Such epigenetic control is often associated with alternative covalent modifications of histones. The stability and heritability of the states are thought to involve positive feedback where modified nucleosomes recruit enzymes that similarly modify nearby nucleosomes. We developed a simplified stochastic model for dynamic nucleosome modification based on the silent mating-type region of the yeast Schizosaccharomyces pombe. We show that the mechanism can give strong bistability that is resistant both to high noise due to random gain or loss of nucleosome modifications and to random partitioning upon DNA replication. However, robust bistability required: (1) cooperativity, the activity of more than one modified nucleosome, in the modification reactions and (2) that nucleosomes occasionally stimulate modification beyond their neighbor nucleosomes, arguing against a simple continuous spreading of nucleosome modification.

No abstract

No abstract

No abstract

Traffic is constrained by the information involved in locating the receiver and the physical distance between sender and receiver. We here focus on the former, and investigate traffic in the perspective of information handling. We replot the road map of cities in terms of the information needed to locate specific addresses and create information city networks with roads mapped to nodes and intersections to links between nodes. These networks have the broad degree distribution found in many other complex networks. The mapping to an information city network makes it possible to quantify the information associated with locating specific addresses.

No abstract