66 research outputs found
Emergence of structural and dynamical properties of ecological mutualistic networks
Mutualistic networks are formed when the interactions between two classes of
species are mutually beneficial. They are important examples of cooperation
shaped by evolution. Mutualism between animals and plants plays a key role in
the organization of ecological communities. Such networks in ecology have
generically evolved a nested architecture independent of species composition
and latitude - specialists interact with proper subsets of the nodes with whom
generalists interact. Despite sustained efforts to explain observed network
structure on the basis of community-level stability or persistence, such
correlative studies have reached minimal consensus. Here we demonstrate that
nested interaction networks could emerge as a consequence of an optimization
principle aimed at maximizing the species abundance in mutualistic communities.
Using analytical and numerical approaches, we show that because of the
mutualistic interactions, an increase in abundance of a given species results
in a corresponding increase in the total number of individuals in the
community, as also the nestedness of the interaction matrix. Indeed, the
species abundances and the nestedness of the interaction matrix are correlated
by an amount that depends on the strength of the mutualistic interactions.
Nestedness and the observed spontaneous emergence of generalist and specialist
species occur for several dynamical implementations of the variational
principle under stationary conditions. Optimized networks, while remaining
stable, tend to be less resilient than their counterparts with randomly
assigned interactions. In particular, we analytically show that the abundance
of the rarest species is directly linked to the resilience of the community.
Our work provides a unifying framework for studying the emergent structural and
dynamical properties of ecological mutualistic networks.Comment: 10 pages, 4 figure
Cooperation and Contagion in Web-Based, Networked Public Goods Experiments
A longstanding idea in the literature on human cooperation is that
cooperation should be reinforced when conditional cooperators are more likely
to interact. In the context of social networks, this idea implies that
cooperation should fare better in highly clustered networks such as cliques
than in networks with low clustering such as random networks. To test this
hypothesis, we conducted a series of web-based experiments, in which 24
individuals played a local public goods game arranged on one of five network
topologies that varied between disconnected cliques and a random regular graph.
In contrast with previous theoretical work, we found that network topology had
no significant effect on average contributions. This result implies either that
individuals are not conditional cooperators, or else that cooperation does not
benefit from positive reinforcement between connected neighbors. We then tested
both of these possibilities in two subsequent series of experiments in which
artificial seed players were introduced, making either full or zero
contributions. First, we found that although players did generally behave like
conditional cooperators, they were as likely to decrease their contributions in
response to low contributing neighbors as they were to increase their
contributions in response to high contributing neighbors. Second, we found that
positive effects of cooperation were contagious only to direct neighbors in the
network. In total we report on 113 human subjects experiments, highlighting the
speed, flexibility, and cost-effectiveness of web-based experiments over those
conducted in physical labs
Calculating Evolutionary Dynamics in Structured Populations
Evolution is shaping the world around us. At the core of every evolutionary process is a population of reproducing individuals. The outcome of an evolutionary process depends on population structure. Here we provide a general formula for calculating evolutionary dynamics in a wide class of structured populations. This class includes the recently introduced “games in phenotype space” and “evolutionary set theory.” There can be local interactions for determining the relative fitness of individuals, but we require global updating, which means all individuals compete uniformly for reproduction. We study the competition of two strategies in the context of an evolutionary game and determine which strategy is favored in the limit of weak selection. We derive an intuitive formula for the structure coefficient, σ, and provide a method for efficient numerical calculation
Mobility promotes and jeopardizes biodiversity in rock-paper-scissors games
Biodiversity is essential to the viability of ecological systems. Species
diversity in ecosystems is promoted by cyclic, non-hierarchical interactions
among competing populations. Such non-transitive relations lead to an evolution
with central features represented by the `rock-paper-scissors' game, where rock
crushes scissors, scissors cut paper, and paper wraps rock. In combination with
spatial dispersal of static populations, this type of competition results in
the stable coexistence of all species and the long-term maintenance of
biodiversity. However, population mobility is a central feature of real
ecosystems: animals migrate, bacteria run and tumble. Here, we observe a
critical influence of mobility on species diversity. When mobility exceeds a
certain value, biodiversity is jeopardized and lost. In contrast, below this
critical threshold all subpopulations coexist and an entanglement of travelling
spiral waves forms in the course of temporal evolution. We establish that this
phenomenon is robust, it does not depend on the details of cyclic competition
or spatial environment. These findings have important implications for
maintenance and evolution of ecological systems and are relevant for the
formation and propagation of patterns in excitable media, such as chemical
kinetics or epidemic outbreaks.Comment: Final submitted version; the printed version can be found at
http://dx.doi.org/10.1038/nature06095 Supplementary movies are available at
http://www.theorie.physik.uni-muenchen.de/lsfrey/images_content/movie1.AVI
and
http://www.theorie.physik.uni-muenchen.de/lsfrey/images_content/movie2.AV
On State-Space Reduction in Multi-Strain Pathogen Models, with an Application to Antigenic Drift in Influenza A
Many pathogens exist in phenotypically distinct strains that interact with each other through competition for hosts. General models that describe such multi-strain systems are extremely difficult to analyze because their state spaces are enormously large. Reduced models have been proposed, but so far all of them necessarily allow for coinfections and require that immunity be mediated solely by reduced infectivity, a potentially problematic assumption. Here, we suggest a new state-space reduction approach that allows immunity to be mediated by either reduced infectivity or reduced susceptibility and that can naturally be used for models with or without coinfections. Our approach utilizes the general framework of status-based models. The cornerstone of our method is the introduction of immunity variables, which describe multi-strain systems more naturally than the traditional tracking of susceptible and infected hosts. Models expressed in this way can be approximated in a natural way by a truncation method that is akin to moment closure, allowing us to sharply reduce the size of the state space, and thus to consider models with many strains in a tractable manner. Applying our method to the phenomenon of antigenic drift in influenza A, we propose a potentially general mechanism that could constrain viral evolution to a one-dimensional manifold in a two-dimensional trait space. Our framework broadens the class of multi-strain systems that can be adequately described by reduced models. It permits computational, and even analytical, investigation and thus serves as a useful tool for understanding the evolution and ecology of multi-strain pathogens
Infectious Disease Modeling of Social Contagion in Networks
Many behavioral phenomena have been found to spread interpersonally through social networks, in a manner similar to infectious diseases. An important difference between social contagion and traditional infectious diseases, however, is that behavioral phenomena can be acquired by non-social mechanisms as well as through social transmission. We introduce a novel theoretical framework for studying these phenomena (the SISa model) by adapting a classic disease model to include the possibility for ‘automatic’ (or ‘spontaneous’) non-social infection. We provide an example of the use of this framework by examining the spread of obesity in the Framingham Heart Study Network. The interaction assumptions of the model are validated using longitudinal network transmission data. We find that the current rate of becoming obese is 2 per year and increases by 0.5 percentage points for each obese social contact. The rate of recovering from obesity is 4 per year, and does not depend on the number of non-obese contacts. The model predicts a long-term obesity prevalence of approximately 42, and can be used to evaluate the effect of different interventions on steady-state obesity. Model predictions quantitatively reproduce the actual historical time course for the prevalence of obesity. We find that since the 1970s, the rate of recovery from obesity has remained relatively constant, while the rates of both spontaneous infection and transmission have steadily increased over time. This suggests that the obesity epidemic may be driven by increasing rates of becoming obese, both spontaneously and transmissively, rather than by decreasing rates of losing weight. A key feature of the SISa model is its ability to characterize the relative importance of social transmission by quantitatively comparing rates of spontaneous versus contagious infection. It provides a theoretical framework for studying the interpersonal spread of any state that may also arise spontaneously, such as emotions, behaviors, health states, ideas or diseases with reservoirs.National Institutes of Health (U.S.) (grant R01GM078986)National Science Foundation (U.S.)Bill & Melinda Gates FoundationTempleton FoundationNational Institute on Aging (grant P01 AG031093)Framingham Heart Study (contract number N01-HC-25195
Towards Predictive Computational Models of Oncolytic Virus Therapy: Basis for Experimental Validation and Model Selection
Oncolytic viruses are viruses that specifically infect cancer cells and kill them, while leaving healthy cells largely intact. Their ability to spread through the tumor makes them an attractive therapy approach. While promising results have been observed in clinical trials, solid success remains elusive since we lack understanding of the basic principles that govern the dynamical interactions between the virus and the cancer. In this respect, computational models can help experimental research at optimizing treatment regimes. Although preliminary mathematical work has been performed, this suffers from the fact that individual models are largely arbitrary and based on biologically uncertain assumptions. Here, we present a general framework to study the dynamics of oncolytic viruses that is independent of uncertain and arbitrary mathematical formulations. We find two categories of dynamics, depending on the assumptions about spatial constraints that govern that spread of the virus from cell to cell. If infected cells are mixed among uninfected cells, there exists a viral replication rate threshold beyond which tumor control is the only outcome. On the other hand, if infected cells are clustered together (e.g. in a solid tumor), then we observe more complicated dynamics in which the outcome of therapy might go either way, depending on the initial number of cells and viruses. We fit our models to previously published experimental data and discuss aspects of model validation, selection, and experimental design. This framework can be used as a basis for model selection and validation in the context of future, more detailed experimental studies. It can further serve as the basis for future, more complex models that take into account other clinically relevant factors such as immune responses
Where Two Are Fighting, the Third Wins: Stronger Selection Facilitates Greater Polymorphism in Traits Conferring Competition-Dispersal Tradeoffs
A major conundrum in evolution is that, despite natural selection, polymorphism is still omnipresent in nature: Numerous species exhibit multiple morphs, namely several abundant values of an important trait. Polymorphism is particularly prevalent in asymmetric traits, which are beneficial to their carrier in disruptive competitive interference but at the same time bear disadvantages in other aspects, such as greater mortality or lower fecundity. Here we focus on asymmetric traits in which a better competitor disperses fewer offspring in the absence of competition. We report a general pattern in which polymorphic populations emerge when disruptive selection increases: The stronger the selection, the greater the number of morphs that evolve. This pattern is general and is insensitive to the form of the fitness function. The pattern is somewhat counterintuitive since directional selection is excepted to sharpen the trait distribution and thereby reduce its diversity (but note that similar patterns were suggested in studies that demonstrated increased biodiversity as local selection increases in ecological communities). We explain the underlying mechanism in which stronger selection drives the population towards more competitive values of the trait, which in turn reduces the population density, thereby enabling lesser competitors to stably persist with reduced need to directly compete. Thus, we believe that the pattern is more general and may apply to asymmetric traits more broadly. This robust pattern suggests a comparative, unified explanation to a variety of polymorphic traits in nature.ope
Critical mutation rate has an exponential dependence on population size for eukaryotic-length genomes with crossover
The critical mutation rate (CMR) determines the shift between survival-of-the-fittest and survival of individuals with greater mutational robustness (“flattest”). We identify an inverse relationship between CMR and sequence length in an in silico system with a two-peak fitness landscape; CMR decreases to no more than five orders of magnitude above estimates of eukaryotic per base mutation rate. We confirm the CMR reduces exponentially at low population sizes, irrespective of peak radius and distance, and increases with the number of genetic crossovers. We also identify an inverse relationship between CMR and the number of genes, confirming that, for a similar number of genes to that for the plant Arabidopsis thaliana (25,000), the CMR is close to its known wild-type mutation rate; mutation rates for additional organisms were also found to be within one order of magnitude of the CMR. This is the first time such a simulation model has been assigned input and produced output within range for a given biological organism. The decrease in CMR with population size previously observed is maintained; there is potential for the model to influence understanding of populations undergoing bottleneck, stress, and conservation strategy for populations near extinction
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