95,337 research outputs found
ModuLand plug-in for Cytoscape: determination of hierarchical layers of overlapping network modules and community centrality
Summary: The ModuLand plug-in provides Cytoscape users an algorithm for
determining extensively overlapping network modules. Moreover, it identifies
several hierarchical layers of modules, where meta-nodes of the higher
hierarchical layer represent modules of the lower layer. The tool assigns
module cores, which predict the function of the whole module, and determines
key nodes bridging two or multiple modules. The plug-in has a detailed
JAVA-based graphical interface with various colouring options. The ModuLand
tool can run on Windows, Linux, or Mac OS. We demonstrate its use on protein
structure and metabolic networks. Availability: The plug-in and its user guide
can be downloaded freely from: http://www.linkgroup.hu/modules.php. Contact:
[email protected] Supplementary information: Supplementary
information is available at Bioinformatics online.Comment: 39 pages, 1 figure and a Supplement with 9 figures and 10 table
Dynamical and Structural Modularity of Discrete Regulatory Networks
A biological regulatory network can be modeled as a discrete function that
contains all available information on network component interactions. From this
function we can derive a graph representation of the network structure as well
as of the dynamics of the system. In this paper we introduce a method to
identify modules of the network that allow us to construct the behavior of the
given function from the dynamics of the modules. Here, it proves useful to
distinguish between dynamical and structural modules, and to define network
modules combining aspects of both. As a key concept we establish the notion of
symbolic steady state, which basically represents a set of states where the
behavior of the given function is in some sense predictable, and which gives
rise to suitable network modules. We apply the method to a regulatory network
involved in T helper cell differentiation
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Revealing Dynamic Mechanisms of Cell Fate Decisions From Single-Cell Transcriptomic Data.
Cell fate decisions play a pivotal role in development, but technologies for dissecting them are limited. We developed a multifunction new method, Topographer, to construct a "quantitative" Waddington's landscape of single-cell transcriptomic data. This method is able to identify complex cell-state transition trajectories and to estimate complex cell-type dynamics characterized by fate and transition probabilities. It also infers both marker gene networks and their dynamic changes as well as dynamic characteristics of transcriptional bursting along the cell-state transition trajectories. Applying this method to single-cell RNA-seq data on the differentiation of primary human myoblasts, we not only identified three known cell types, but also estimated both their fate probabilities and transition probabilities among them. We found that the percent of genes expressed in a bursty manner is significantly higher at (or near) the branch point (~97%) than before or after branch (below 80%), and that both gene-gene and cell-cell correlation degrees are apparently lower near the branch point than away from the branching. Topographer allows revealing of cell fate mechanisms in a coherent way at three scales: cell lineage (macroscopic), gene network (mesoscopic), and gene expression (microscopic)
Multilevel compression of random walks on networks reveals hierarchical organization in large integrated systems
To comprehend the hierarchical organization of large integrated systems, we
introduce the hierarchical map equation, which reveals multilevel structures in
networks. In this information-theoretic approach, we exploit the duality
between compression and pattern detection; by compressing a description of a
random walker as a proxy for real flow on a network, we find regularities in
the network that induce this system-wide flow. Finding the shortest multilevel
description of the random walker therefore gives us the best hierarchical
clustering of the network, the optimal number of levels and modular partition
at each level, with respect to the dynamics on the network. With a novel search
algorithm, we extract and illustrate the rich multilevel organization of
several large social and biological networks. For example, from the global air
traffic network we uncover countries and continents, and from the pattern of
scientific communication we reveal more than 100 scientific fields organized in
four major disciplines: life sciences, physical sciences, ecology and earth
sciences, and social sciences. In general, we find shallow hierarchical
structures in globally interconnected systems, such as neural networks, and
rich multilevel organizations in systems with highly separated regions, such as
road networks.Comment: 11 pages, 5 figures. For associated code, see
http://www.tp.umu.se/~rosvall/code.htm
Theories for influencer identification in complex networks
In social and biological systems, the structural heterogeneity of interaction
networks gives rise to the emergence of a small set of influential nodes, or
influencers, in a series of dynamical processes. Although much smaller than the
entire network, these influencers were observed to be able to shape the
collective dynamics of large populations in different contexts. As such, the
successful identification of influencers should have profound implications in
various real-world spreading dynamics such as viral marketing, epidemic
outbreaks and cascading failure. In this chapter, we first summarize the
centrality-based approach in finding single influencers in complex networks,
and then discuss the more complicated problem of locating multiple influencers
from a collective point of view. Progress rooted in collective influence
theory, belief-propagation and computer science will be presented. Finally, we
present some applications of influencer identification in diverse real-world
systems, including online social platforms, scientific publication, brain
networks and socioeconomic systems.Comment: 24 pages, 6 figure
Detection of regulator genes and eQTLs in gene networks
Genetic differences between individuals associated to quantitative phenotypic
traits, including disease states, are usually found in non-coding genomic
regions. These genetic variants are often also associated to differences in
expression levels of nearby genes (they are "expression quantitative trait
loci" or eQTLs for short) and presumably play a gene regulatory role, affecting
the status of molecular networks of interacting genes, proteins and
metabolites. Computational systems biology approaches to reconstruct causal
gene networks from large-scale omics data have therefore become essential to
understand the structure of networks controlled by eQTLs together with other
regulatory genes, and to generate detailed hypotheses about the molecular
mechanisms that lead from genotype to phenotype. Here we review the main
analytical methods and softwares to identify eQTLs and their associated genes,
to reconstruct co-expression networks and modules, to reconstruct causal
Bayesian gene and module networks, and to validate predicted networks in
silico.Comment: minor revision with typos corrected; review article; 24 pages, 2
figure
Identifying modular flows on multilayer networks reveals highly overlapping organization in social systems
Unveiling the community structure of networks is a powerful methodology to
comprehend interconnected systems across the social and natural sciences. To
identify different types of functional modules in interaction data aggregated
in a single network layer, researchers have developed many powerful methods.
For example, flow-based methods have proven useful for identifying modular
dynamics in weighted and directed networks that capture constraints on flow in
the systems they represent. However, many networked systems consist of agents
or components that exhibit multiple layers of interactions. Inevitably,
representing this intricate network of networks as a single aggregated network
leads to information loss and may obscure the actual organization. Here we
propose a method based on compression of network flows that can identify
modular flows in non-aggregated multilayer networks. Our numerical experiments
on synthetic networks show that the method can accurately identify modules that
cannot be identified in aggregated networks or by analyzing the layers
separately. We capitalize on our findings and reveal the community structure of
two multilayer collaboration networks: scientists affiliated to the Pierre
Auger Observatory and scientists publishing works on networks on the arXiv.
Compared to conventional aggregated methods, the multilayer method reveals
smaller modules with more overlap that better capture the actual organization
Network-based approaches to explore complex biological systems towards network medicine
Network medicine relies on different types of networks: from the molecular level of protein–protein interactions to gene regulatory network and correlation studies of gene expression. Among network approaches based on the analysis of the topological properties of protein–protein interaction (PPI) networks, we discuss the widespread DIAMOnD (disease module detection) algorithm. Starting from the assumption that PPI networks can be viewed as maps where diseases can be identified with localized perturbation within a specific neighborhood (i.e., disease modules), DIAMOnD performs a systematic analysis of the human PPI network to uncover new disease-associated genes by exploiting the connectivity significance instead of connection density. The past few years have witnessed the increasing interest in understanding the molecular mechanism of post-transcriptional regulation with a special emphasis on non-coding RNAs since they are emerging as key regulators of many cellular processes in both physiological and pathological states. Recent findings show that coding genes are not the only targets that microRNAs interact with. In fact, there is a pool of different RNAs—including long non-coding RNAs (lncRNAs) —competing with each other to attract microRNAs for interactions, thus acting as competing endogenous RNAs (ceRNAs). The framework of regulatory networks provides a powerful tool to gather new insights into ceRNA regulatory mechanisms. Here, we describe a data-driven model recently developed to explore the lncRNA-associated ceRNA activity in breast invasive carcinoma. On the other hand, a very promising example of the co-expression network is the one implemented by the software SWIM (switch miner), which combines topological properties of correlation networks with gene expression data in order to identify a small pool of genes—called switch genes—critically associated with drastic changes in cell phenotype. Here, we describe SWIM tool along with its applications to cancer research and compare its predictions with DIAMOnD disease genes
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