Bipartite networks are a common type of network data in which there are two types of vertices, and only vertices of different types can be connected. While bipartite networks exhibit community structure like their unipartite counterparts, existing ap
proaches to bipartite community detection have drawbacks, including implicit parameter choices, loss of information through one-mode projections, and lack of interpretability. Here we solve the community detection problem for bipartite networks by formulating a bipartite stochastic block model, which explicitly includes vertex type information and may be trivially extended to $k$-partite networks. This bipartite stochastic block model yields a projection-free and statistically principled method for community detection that makes clear assumptions and parameter choices and yields interpretable results. We demonstrate this models ability to efficiently and accurately find community structure in synthetic bipartite networks with known structure and in real-world bipartite networks with unknown structure, and we characterize its performance in practical contexts.
The var genes of the human malaria parasite Plasmodium falciparum present a challenge to population geneticists due to their extreme diversity, which is generated by high rates of recombination. These genes encode a primary antigen protein called PfE
MP1, which is expressed on the surface of infected red blood cells and elicits protective immune responses. Var gene sequences are characterized by pronounced mosaicism, precluding the use of traditional phylogenetic tools that require bifurcating tree-like evolutionary relationships. We present a new method that identifies highly variable regions (HVRs), and then maps each HVR to a complex network in which each sequence is a node and two nodes are linked if they share an exact match of significant length. Here, networks of var genes that recombine freely are expected to have a uniformly random structure, but constraints on recombination will produce network communities that we identify using a stochastic block model. We validate this method on synthetic data, showing that it correctly recovers populations of constrained recombination, before applying it to the Duffy Binding Like-{alpha} (DBL{alpha}) domain of var genes. We find nine HVRs whose network communities map in distinctive ways to known DBL{alpha} classifications and clinical phenotypes. We show that the recombinational constraints of some HVRs are correlated, while others are independent. These findings suggest that this micromodular structuring facilitates independent evolutionary trajectories of neighboring mosaic regions, allowing the parasite to retain protein function while generating enormous sequence diversity. Our approach therefore offers a rigorous method for analyzing evolutionary constraints in var genes, and is also flexible enough to be easily applied more generally to any highly recombinant sequences.
The collective dynamics of a network of excitable nodes changes dramatically when inhibitory nodes are introduced. We consider inhibitory nodes which may be activated just like excitatory nodes but, upon activating, decrease the probability of activa
tion of network neighbors. We show that, although the direct effect of inhibitory nodes is to decrease activity, the collective dynamics becomes self-sustaining. We explain this counterintuitive result by defining and analyzing a branching function which may be thought of as an activity-dependent branching ratio. The shape of the branching function implies that for a range of global coupling parameters dynamics are self-sustaining. Within the self-sustaining region of parameter space lies a critical line along which dynamics take the form of avalanches with universal scaling of size and duration, embedded in ceaseless timeseries of activity. Our analyses, confirmed by numerical simulation, suggest that inhibition may play a counterintuitive role in excitable networks.
We characterize the distributions of size and duration of avalanches propagating in complex networks. By an avalanche we mean the sequence of events initiated by the externally stimulated `excitation of a network node, which may, with some probabilit
y, then stimulate subsequent firings of the nodes to which it is connected, resulting in a cascade of firings. This type of process is relevant to a wide variety of situations, including neuroscience, cascading failures on electrical power grids, and epidemology. We find that the statistics of avalanches can be characterized in terms of the largest eigenvalue and corresponding eigenvector of an appropriate adjacency matrix which encodes the structure of the network. By using mean-field analyses, previous studies of avalanches in networks have not considered the effect of network structure on the distribution of size and duration of avalanches. Our results apply to individual networks (rather than network ensembles) and provide expressions for the distributions of size and duration of avalanches starting at particular nodes in the network. These findings might find application in the analysis of branching processes in networks, such as cascading power grid failures and critical brain dynamics. In particular, our results show that some experimental signatures of critical brain dynamics (i.e., power-law distributions of size and duration of neuronal avalanches), are robust to complex underlying network topologies.
