The topological analysis of biological networks has been a prolific topic in network science during the last decade. A persistent problem with this approach is the inherent uncertainty and noisy nature of the data. One of the cases in which this situ
ation is more marked is that of transcriptional regulatory networks (TRNs) in bacteria. The datasets are incomplete because regulatory pathways associated to a relevant fraction of bacterial genes remain unknown. Furthermore, direction, strengths and signs of the links are sometimes unknown or simply overlooked. Finally, the experimental approaches to infer the regulations are highly heterogeneous, in a way that induces the appearance of systematic experimental-topological correlations. And yet, the quality of the available data increases constantly. In this work we capitalize on these advances to point out the influence of data (in)completeness and quality on some classical results on topological analysis of TRNs, specially regarding modularity at different levels. In doing so, we identify the most relevant factors affecting the validity of previous findings, highlighting important caveats to future prokaryotic TRNs topological analysis.
Many epidemic processes in networks spread by stochastic contacts among their connected vertices. There are two limiting cases widely analyzed in the physics literature, the so-called contact process (CP) where the contagion is expanded at a certain
rate from an infected vertex to one neighbor at a time, and the reactive process (RP) in which an infected individual effectively contacts all its neighbors to expand the epidemics. However, a more realistic scenario is obtained from the interpolation between these two cases, considering a certain number of stochastic contacts per unit time. Here we propose a discrete-time formulation of the problem of contact-based epidemic spreading. We resolve a family of models, parameterized by the number of stochastic contact trials per unit time, that range from the CP to the RP. In contrast to the common heterogeneous mean-field approach, we focus on the probability of infection of individual nodes. Using this formulation, we can construct the whole phase diagram of the different infection models and determine their critical properties.
