Merging Arcs to Produce Acyclic Phylogenetic Networks and Normal Networks

As phylogenetic networks grow increasingly complicated, systematic methods for simplifying them to reveal properties will become more useful. This paper considers how to modify acyclic phylogenetic networks into other acyclic networks by contracting specific arcs that include a set D. The networks need not be binary, so vertices in the networks may have more than two parents and/or more than two children. In general, in order to make the resulting network acyclic, additional arcs not in D must also be contracted. This paper shows how to choose D so that the resulting acyclic network is “pre-normal”. As a result, removal of all redundant arcs yields a normal network. The set D can be selected based only on the geometry of the network, giving a well-defined normal phylogenetic network depending only on the given network. There are CSD maps relating most of the networks. The resulting network can be visualized as a “wired lift” in the original network, which appears as the original network with each arc drawn in one of three ways.

Display Sets of Normal and Tree-Child Networks

Phylogenetic networks are leaf-labelled directed acyclic graphs that are used in computational biology to analyse and represent the evolutionary relationships of a set of species or viruses. In contrast to phylogenetic trees, phylogenetic networks have vertices of in-degree at least two that represent reticulation events such as hybridisation, lateral gene transfer, or reassortment. By systematically deleting various combinations of arcs in a phylogenetic network $\mathcal N$, one derives a set of phylogenetic trees that are embedded in $\mathcal N$. We recently showed that the problem of deciding if two binary phylogenetic networks embed the same set of phylogenetic trees is computationally hard, in particular, we showed it to be $\Pi^P_2$-complete. In this paper, we establish a polynomial-time algorithm for this decision problem if the initial two networks consist of a normal network and a tree-child network; two well-studied topologically restricted subclasses of phylogenetic networks, with normal networks being more structurally constrained than tree-child networks. The running time of the algorithm is quadratic in the size of the leaf sets.

Synchronization Dynamics in Non-Normal Networks: The Trade-Off for Optimality

Synchronization is an important behavior that characterizes many natural and human made systems that are composed by several interacting units. It can be found in a broad spectrum of applications, ranging from neuroscience to power-grids, to mention a few. Such systems synchronize because of the complex set of coupling they exhibit, with the latter being modeled by complex networks. The dynamical behavior of the system and the topology of the underlying network are strongly intertwined, raising the question of the optimal architecture that makes synchronization robust. The Master Stability Function (MSF) has been proposed and extensively studied as a generic framework for tackling synchronization problems. Using this method, it has been shown that, for a class of models, synchronization in strongly directed networks is robust to external perturbations. Recent findings indicate that many real-world networks are strongly directed, being potential candidates for optimal synchronization. Moreover, many empirical networks are also strongly non-normal. Inspired by this latter fact in this work, we address the role of the non-normality in the synchronization dynamics by pointing out that standard techniques, such as the MSF, may fail to predict the stability of synchronized states. We demonstrate that, due to a transient growth that is induced by the structure’s non-normality, the system might lose synchronization, contrary to the spectral prediction. These results lead to a trade-off between non-normality and directedness that should be properly considered when designing an optimal network, enhancing the robustness of synchronization.

Efficient communication over complex dynamical networks: The role of matrix non-normality

In both natural and engineered systems, communication often occurs dynamically over networks ranging from highly structured grids to largely disordered graphs. To use, or comprehend the use of, networks as efficient communication media requires understanding of how they propagate and transform information in the face of noise. Here, we develop a framework that enables us to examine how network structure, noise, and interference between consecutive packets jointly determine transmission performance in complex networks governed by linear dynamics. Mathematically, normal networks, which can be decomposed into separate low-dimensional information channels, suffer greatly from readout noise. Most details of their wiring have no impact on transmission quality. Non-normal networks, however, can largely cancel the effect of noise by transiently amplifying select input dimensions while ignoring others, resulting in higher net information throughput. Our theory could inform the design of new communication networks, as well as the optimal use of existing ones.

Generating normal networks via leaf insertion and nearest neighbor interchange

Background Galled trees are studied as a recombination model in theoretical population genetics. This class of phylogenetic networks has been generalized to tree-child networks and other network classes by relaxing a structural condition imposed on galled trees. Although these networks are simple, their topological structures have yet to be fully understood. Results It is well-known that all phylogenetic trees on n taxa can be generated by the insertion of the n-th taxa to each edge of all the phylogenetic trees on n−1 taxa. We prove that all tree-child (resp. normal) networks with k reticulate nodes on n taxa can be uniquely generated via three operations from all the tree-child (resp. normal) networks with k−1 or k reticulate nodes on n−1 taxa. Applying this result to counting rooted phylogenetic networks, we show that there are exactly $\frac {(2n)!}{2^{n} (n-1)!}-2^{n-1} n!$(2n)!2n(n−1)!−2n−1n! binary phylogenetic networks with one reticulate node on n taxa. Conclusions The work makes two contributions to understand normal networks. One is a generalization of an enumeration procedure for phylogenetic trees into one for normal networks. Another is simple formulas for counting normal networks and phylogenetic networks that have only one reticulate node.

Structure and dynamical behavior of non-normal networks

We analyze a collection of empirical networks in a wide spectrum of disciplines and show that strong non-normality is ubiquitous in network science. Dynamical processes evolving on non-normal networks exhibit a peculiar behavior, as initial small disturbances may undergo a transient phase and be strongly amplified in linearly stable systems. In addition, eigenvalues may become extremely sensible to noise and have a diminished physical meaning. We identify structural properties of networks that are associated with non-normality and propose simple models to generate networks with a tunable level of non-normality. We also show the potential use of a variety of metrics capturing different aspects of non-normality and propose their potential use in the context of the stability of complex ecosystems.

A Comprehensive Survey of Immune Cytolytic Activity-Associated Gene Co-Expression Networks across 17 Tumor and Normal Tissue Types

Cytolytic immune activity in solid tissue can be quantified by transcript levels of two genes, GZMA and PRF1, which is named the CYT score. A previous study has investigated the molecular and genetic properties of tumors associated CYT, but a systematic exploration of how co-expression networks across different tumors are shaped by anti-tumor immunity is lacking. Here, we examined the connectivity and biological themes of CYT-associated modules in gene co-expression networks of 14 tumor and 3 matched normal tissues constructed from the RNA-Seq data of the “The Cancer Genome Atlas” project. We first found that tumors networks have more diverse CYT-correlated modules than normal networks. We next identified and investigated tissue-specific CYT-associated modules across 14 tumor types. Finally, a common CYT-associated network across 14 tumor types was constructed. Two common modules have mixed signs of correlation with CYT in different tumors. Given the tumors and normal tissues surveyed, our study presents a systematic view of the regulation of cytolytic immune activity across multiple tumor tissues.