Secluded Connectivity Problems

Consider a setting where possibly sensitive information sent over a path in a network is visible to every {neighbor} of the path, i.e., every neighbor of some node on the path, thus including the nodes on the path itself. The exposure of a path $P$ can be measured as the number of nodes adjacent to it, denoted by $N[P]$. A path is said to be secluded if its exposure is small. A similar measure can be applied to other connected subgraphs, such as Steiner trees connecting a given set of terminals. Such subgraphs may be relevant due to considerations of privacy, security or revenue maximization. This paper considers problems related to minimum exposure connectivity structures such as paths and Steiner trees. It is shown that on unweighted undirected $n$-node graphs, the problem of finding the minimum exposure path connecting a given pair of vertices is strongly inapproximable, i.e., hard to approximate within a factor of $O(2^{\log^{1-\epsilon}n})$ for any $\epsilon>0$ (under an appropriate complexity assumption), but is approximable with ratio $\sqrt{\Delta}+3$, where $\Delta$ is the maximum degree in the graph. One of our main results concerns the class of bounded-degree graphs, which is shown to exhibit the following interesting dichotomy. On the one hand, the minimum exposure path problem is NP-hard on node-weighted or directed bounded-degree graphs (even when the maximum degree is 4). On the other hand, we present a polynomial algorithm (based on a nontrivial dynamic program) for the problem on unweighted undirected bounded-degree graphs. Likewise, the problem is shown to be polynomial also for the class of (weighted or unweighted) bounded-treewidth graphs

Vertex Fault Tolerant Additive Spanners

A {\em fault-tolerant} structure for a network is required to continue functioning following the failure of some of the network's edges or vertices. In this paper, we address the problem of designing a {\em fault-tolerant} additive spanner, namely, a subgraph $H$ of the network $G$ such that subsequent to the failure of a single vertex, the surviving part of $H$ still contains an \emph{additive} spanner for (the surviving part of) $G$, satisfying $dist(s,t,H\setminus \{v\}) \leq dist(s,t,G\setminus \{v\})+\beta$ for every $s,t,v \in V$. Recently, the problem of constructing fault-tolerant additive spanners resilient to the failure of up to $f$ \emph{edges} has been considered by Braunschvig et. al. The problem of handling \emph{vertex} failures was left open therein. In this paper we develop new techniques for constructing additive FT-spanners overcoming the failure of a single vertex in the graph. Our first result is an FT-spanner with additive stretch $2$ and $\widetilde{O}(n^{5/3})$ edges. Our second result is an FT-spanner with additive stretch $6$ and $\widetilde{O}(n^{3/2})$ edges. The construction algorithm consists of two main components: (a) constructing an FT-clustering graph and (b) applying a modified path-buying procedure suitably adopted to failure prone settings. Finally, we also describe two constructions for {\em fault-tolerant multi-source additive spanners}, aiming to guarantee a bounded additive stretch following a vertex failure, for every pair of vertices in $S \times V$ for a given subset of sources $S\subseteq V$. The additive stretch bounds of our constructions are 4 and 8 (using a different number of edges)

A statistical mechanics description of environmental variability in metabolic networks

Many of the chemical reactions that take place within a living cell are irreversible. Due to evolutionary pressures, the number of allowable reactions within these systems are highly constrained and thus the resulting metabolic networks display considerable asymmetry. In this paper, we explore possible evolutionary factors pertaining to the reduced symmetry observed in these networks, and demonstrate the important role environmental variability plays in shaping their structural organization. Interpreting the returnability index as an equilibrium constant for a reaction network in equilibrium with a hypothetical reference system, enables us to quantify the extent to which a metabolic network is in disequilibrium. Further, by introducing a new directed centrality measure via an extension of the subgraph centrality metric to directed networks, we are able to characterise individual metabolites by their participation within metabolic pathways. To demonstrate these ideas, we study 116 metabolic networks of bacteria. In particular, we find that the equilibrium constant for the metabolic networks decreases significantly in-line with variability in bacterial habitats, supporting the view that environmental variability promotes disequilibrium within these biochemical reaction system

Evolution of associative learning in chemical networks

Organisms that can learn about their environment and modify their behaviour appropriately during their lifetime are more likely to survive and reproduce than organisms that do not. While associative learning – the ability to detect correlated features of the environment – has been studied extensively in nervous systems, where the underlying mechanisms are reasonably well understood, mechanisms within single cells that could allow associative learning have received little attention. Here, using in silico evolution of chemical networks, we show that there exists a diversity of remarkably simple and plausible chemical solutions to the associative learning problem, the simplest of which uses only one core chemical reaction. We then asked to what extent a linear combination of chemical concentrations in the network could approximate the ideal Bayesian posterior of an environment given the stimulus history so far? This Bayesian analysis revealed the ’memory traces’ of the chemical network. The implication of this paper is that there is little reason to believe that a lack of suitable phenotypic variation would prevent associative learning from evolving in cell signalling, metabolic, gene regulatory, or a mixture of these networks in cells

Evolutionary connectionism: algorithmic principles underlying the evolution of biological organisation in evo-devo, evo-eco and evolutionary transitions

The mechanisms of variation, selection and inheritance, on which evolution by natural selection depends, are not fixed over evolutionary time. Current evolutionary biology is increasingly focussed on understanding how the evolution of developmental organisations modifies the distribution of phenotypic variation, the evolution of ecological relationships modifies the selective environment, and the evolution of reproductive relationships modifies the heritability of the evolutionary unit. The major transitions in evolution, in particular, involve radical changes in developmental, ecological and reproductive organisations that instantiate variation, selection and inheritance at a higher level of biological organisation. However, current evolutionary theory is poorly equipped to describe how these organisations change over evolutionary time and especially how that results in adaptive complexes at successive scales of organisation (the key problem is that evolution is self-referential, i.e. the products of evolution change the parameters of the evolutionary process). Here we first reinterpret the central open questions in these domains from a perspective that emphasises the common underlying themes. We then synthesise the findings from a developing body of work that is building a new theoretical approach to these questions by converting well-understood theory and results from models of cognitive learning. Specifically, connectionist models of memory and learning demonstrate how simple incremental mechanisms, adjusting the relationships between individually-simple components, can produce organisations that exhibit complex system-level behaviours and improve the adaptive capabilities of the system. We use the term “evolutionary connectionism” to recognise that, by functionally equivalent processes, natural selection acting on the relationships within and between evolutionary entities can result in organisations that produce complex system-level behaviours in evolutionary systems and modify the adaptive capabilities of natural selection over time. We review the evidence supporting the functional equivalences between the domains of learning and of evolution, and discuss the potential for this to resolve conceptual problems in our understanding of the evolution of developmental, ecological and reproductive organisations and, in particular, the major evolutionary transitions

Facilitated Variation: How Evolution Learns from Past Environments To Generalize to New Environments

One of the striking features of evolution is the appearance of novel structures in organisms. Recently, Kirschner and Gerhart have integrated discoveries in evolution, genetics, and developmental biology to form a theory of facilitated variation (FV). The key observation is that organisms are designed such that random genetic changes are channeled in phenotypic directions that are potentially useful. An open question is how FV spontaneously emerges during evolution. Here, we address this by means of computer simulations of two well-studied model systems, logic circuits and RNA secondary structure. We find that evolution of FV is enhanced in environments that change from time to time in a systematic way: the varying environments are made of the same set of subgoals but in different combinations. We find that organisms that evolve under such varying goals not only remember their history but also generalize to future environments, exhibiting high adaptability to novel goals. Rapid adaptation is seen to goals composed of the same subgoals in novel combinations, and to goals where one of the subgoals was never seen in the history of the organism. The mechanisms for such enhanced generation of novelty (generalization) are analyzed, as is the way that organisms store information in their genomes about their past environments. Elements of facilitated variation theory, such as weak regulatory linkage, modularity, and reduced pleiotropy of mutations, evolve spontaneously under these conditions. Thus, environments that change in a systematic, modular fashion seem to promote facilitated variation and allow evolution to generalize to novel conditions

An Analytically Solvable Model for Rapid Evolution of Modular Structure

Biological systems often display modularity, in the sense that they can be decomposed into nearly independent subsystems. Recent studies have suggested that modular structure can spontaneously emerge if goals (environments) change over time, such that each new goal shares the same set of sub-problems with previous goals. Such modularly varying goals can also dramatically speed up evolution, relative to evolution under a constant goal. These studies were based on simulations of model systems, such as logic circuits and RNA structure, which are generally not easy to treat analytically. We present, here, a simple model for evolution under modularly varying goals that can be solved analytically. This model helps to understand some of the fundamental mechanisms that lead to rapid emergence of modular structure under modularly varying goals. In particular, the model suggests a mechanism for the dramatic speedup in evolution observed under such temporally varying goals

Origin of structural difference in metabolic networks with respect to temperature

<p>Abstract</p> <p>Background</p> <p>Metabolism is believed to adaptively shape-shift with changing environment. In recent years, a structural difference with respect to temperature, which is an environmental factor, has been revealed in metabolic networks, implying that metabolic networks transit with temperature. Subsequently, elucidatation of the origin of these structural differences due to temperature is important for understanding the evolution of life. However, the origin has yet to be clarified due to the complexity of metabolic networks.</p> <p>Results</p> <p>Consequently, we propose a simple model with a few parameters to explain the transitions. We first present mathematical solutions of this model using mean-field approximation, and demonstrate that this model can reproduce structural properties, such as heterogeneous connectivity and hierarchical modularity, in real metabolic networks both qualitatively and quantitatively. We next show that the model parameters correlate with optimal growth temperature. In addition, we present a relationship between multiple cyclic properties and optimal growth temperature in metabolic networks.</p> <p>Conclusion</p> <p>From the proposed model, we find that such structural properties are determined by the emergence of a short-cut path, which reduces the minimum distance between two nodes on a graph. Furthermore, we investigate correlations between model parameters and growth temperature; as a result, we find that the emergence of the short-cut path tends to be inhibited with increasing temperature. In addition, we also find that the short-cut path bypasses a relatively long path at high temperature when the emergence of the new path is not inhibited. Even further, additional network analysis provides convincing evidence of the reliability of the proposed model and its conclusions on the possible origins of differences in metabolic network structure.</p