Bulletin of the American Physical Society
APS March Meeting 2014
Volume 59, Number 1
Monday–Friday, March 3–7, 2014; Denver, Colorado
Session Q10: Focus Session: Evolution, Co-evolution, and Game Theory |
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Sponsoring Units: DBIO GSNP Chair: Alexandre Morozov, Rutgers University Room: 201 |
Wednesday, March 5, 2014 2:30PM - 3:06PM |
Q10.00001: Fluctuation-induced patterns and rapid evolution in predator-prey ecosystems Invited Speaker: Nigel Goldenfeld Predator-prey ecosystems exhibit noisy, persistent cycles that cannot be described by intuitive population-level differential equations such as the Lotka-Volterra equations. Traditionally this paradox has been met by including additional nonlinearities such as predator satiation to force limit cycle behavior. Over the last few years, it has been realized that individual-level descriptions, combined with systematic perturbation techniques can reproduce the key features of such systems in a minimal way, without requiring many additional assumptions or fine tunings. Here I review work in this area that uses these techniques to treat spatial patterns and the phenomenon of rapidly evolving prey sub-populations. In the latter case, I show how stochastic individual-level models reproduce the key features observed in chemostats and in the wild, including anomalous phase shifts between predator and prey species, evolutionary cycles and cryptic cycles. This work shows that stochastic individual-level models naturally describe systems where evolutionary time scales surprisingly match ecosystem time scales. [Preview Abstract] |
Wednesday, March 5, 2014 3:06PM - 3:18PM |
Q10.00002: Solutions to the public goods dilemma in bacterial biofilms Knut Drescher, Carey D. Nadell, Howard A. Stone, Ned S. Wingreen, Bonnie L. Bassler Bacteria frequently live in densely populated surface-bound communities, termed biofilms. Biofilm-dwelling cells rely on secretion of extracellular substances to construct their communities and to capture nutrients from the environment. Some secreted factors behave as cooperative public goods: they can be exploited by non-producing cells. The means by which public-good-producing bacteria avert exploitation in biofilm environments are largely unknown. Using experiments with \textit{Vibrio cholerae}, which secretes extracellular enzymes to digest its primary food source, the solid polymer chitin, we show that the public goods dilemma may be solved by two very different mechanisms: cells can produce thick biofilms that confine the goods to producers, or fluid flow can remove soluble products of chitin digestion, denying access to non-producers. Both processes are unified by limiting the distance over which enzyme-secreting cells provide benefits to neighbors, resulting in preferential benefit to nearby clonemates and allowing kin selection to favor public good production. Our results demonstrate new mechanisms by which the physical conditions of natural habitats can interact with bacterial physiology to promote the evolution of cooperation. [Preview Abstract] |
Wednesday, March 5, 2014 3:18PM - 3:30PM |
Q10.00003: Beating Cheaters at Their Own Game Joseph Rauch, Jane Kondev, Alvaro Sanchez Public goods games occur over many different scales in nature, from microbial biofilms to the human commons. On each scale stable populations of cooperators (members who invest into producing some good shared by the entire population) and cheaters (members who make no investment yet still share the common goods) has been observed. This observation raises interesting questions, like how do cooperators maintain their presence in a game that seems to heavily favor cheaters, and what strategies for cooperation could populations employ to increase their success? We propose a model of a public goods game with two different player populations, S and D, which employ two different strategies: the D population always cheats and the S population makes a stochastic decision whether to cooperate or not. We find that stochastic cooperation improves the success of the S population over the competing D population, but at a price. As the probability of cheating by the S players increases they outcompete the D players but the total population becomes more ecologically unstable (i.e., the likelihood of its extinction grows). We investigate this trade off between evolutionary success and ecological stability and propose experiments using populations of yeast cells to test our predictions. [Preview Abstract] |
Wednesday, March 5, 2014 3:30PM - 3:42PM |
Q10.00004: Stability of Zero-Sum Games in Evolutionary Game Theory Johannes Knebel, Torben Krueger, Markus F. Weber, Erwin Frey Evolutionary game theory has evolved into a successful theoretical concept to study mechanisms that govern the evolution of ecological communities. On a mathematical level, this theory was formalized in the framework of the celebrated replicator equations (REs) and its stochastic generalizations. In our work, we analyze the long-time behavior of the REs for zero-sum games with arbitrarily many strategies, which are generalized versions of the children's game Rock-Paper-Scissors.\footnote{J. Knebel, T. Krueger, M.F. Weber, E. Frey, Phys. Rev. Lett. 110, 168106 (2013).} We demonstrate how to determine the strategies that survive and those that become extinct in the long run. Our results show that extinction of strategies is exponentially fast in generic setups, and that conditions for the survival can be formulated in terms of the Pfaffian of the REs' antisymmetric payoff matrix. Consequences for the stochastic dynamics, which arise in finite populations, are reflected by a generalized scaling law for the extinction time in the vicinity of critical reaction rates. Our findings underline the relevance of zero-sum games as a reference for the analysis of other models in evolutionary game theory. [Preview Abstract] |
Wednesday, March 5, 2014 3:42PM - 3:54PM |
Q10.00005: Dynamics of Coevolution and Branching in the Immune System Kimberly Schlesinger, Sean Stromberg, Jean Carlson We investigate the dynamics of coevolution between two coupled populations, in the context of the interaction between mutating pathogen and the adaptive immune response. Our model represents the binding affinities between antigen epitopes and lymphocyte receptors which mediate the interactions of the two populations, and which may change with pathogen mutation. We see diverse possible outcomes of infection, including early pathogen clearance, early pathogen escape from immune control, and an intermediate state of chronic infection, in which pathogen strains coexist with lymphocytes at relatively stable levels. The coevolutionary dynamics within this chronic infection state display emergent structure, including evolutionary branching that is fundamentally driven by the coevolutionary interaction and that results in the clustering of the pathogen population into distinct and independently evolving clusters. The increased fragility of the immune system as it distributes its resources to control a growing number of clusters can lead to the sudden out-of-control growth of the pathogen after months or years of chronic infection. [Preview Abstract] |
Wednesday, March 5, 2014 3:54PM - 4:06PM |
Q10.00006: An obligatory bacterial mutualism in a multi-drug environment exhibits strong oscillatory population dynamics Arolyn Conwill, Eugene Yurtsev, Jeff Gore A common mechanism of antibiotic resistance in bacteria involves the production of an enzyme that inactivates the antibiotic. By inactivating the antibiotic, resistant cells can protect other cells in the population that would otherwise be sensitive to the drug. In a multidrug environment, an obligatory mutualism arises because populations of different strains rely on each other to breakdown antibiotics in the environment. Here, we experimentally track the population dynamics of two \textit{E. coli} strains in the presence of two different antibiotics: ampicillin and chloramphenicol. Together the strains are able to grow in antibiotic concentrations that inhibit growth of either one of the strains alone. Although mutualisms are often thought to stabilize population dynamics, we observe strong oscillatory dynamics even when there is long-term coexistence between the two strains. We expect that our results will provide insight into the evolution of antibiotic resistance and, more generally, the evolutionary origin of phenotypic diversity, cooperation, and ecological stability. [Preview Abstract] |
Wednesday, March 5, 2014 4:06PM - 4:42PM |
Q10.00007: Survivial Strategies in Bacterial Range Expansions Invited Speaker: Erwin Frey Bacterial communities represent complex and dynamic ecological~systems. Different environmental conditions as well~as bacterial~interactions determine the establishment and sustainability of bacterial diversity. In~this talk we discuss the~competition of three Escherichia coli~strains during range expansions on agar plates. In this bacterial model~system, a~colicin E2 producing strain C competes with a colicin~resistant strain R and with a colicin sensitive strain S for new~territory. Genetic engineering allows us to tune the growth rates of the~strains and to study distinct ecological scenarios.~These scenarios may~lead to either single-strain dominance, pairwise coexistence, or to the coexistence of~all three~strains. In order to elucidate the survival mechanisms of the~individual strains, we also developed a stochastic agent-based model to~capture the ecological scenarios in silico. In a combined theoretical and~experimental approach we are~able to show that the level of~biodiversity depends crucially on the composition of the inoculum, on~the relative growth~rates of the three strains, and on the effective reach~of colicin toxicity. [Preview Abstract] |
Wednesday, March 5, 2014 4:42PM - 4:54PM |
Q10.00008: Widespread Attenuation of Antibiotics by Soil Bacteria Promotes Intermixed Microbial Diversity Kalin Vetsigin, Eric Kelsic, Jeffrey Zhao, Roy Kishony In natural soil environments, antibiotic sensitive bacteria coexist with antibiotic producers, even in close proximities. Efforts to understand diversity in microbial communities have focused on pairwise interactions between species, yet mathematical models of such interactions lead to distinct spatial domains of individual species, rather than to intermixed multi-species communities. In this work, we measured interactions between triplets of species and asked and how the presence of these higher-order interactions affects community structure and diversity. We developed a 3-species diffusion-based assay in which a modulator species either intensifies or attenuates the toxicity of compounds made by a producer species against a fluorescently labeled indicator species. We found that intensifying interactions were quite rare among soil bacteria, while attenuating interactions that protected nearby sensitive species from the antibiotic producer were abundant. Furthermore, many soil bacteria attenuated multiple classes of antibiotics with widely varying mechanisms of action. Computer simulations showed that such cross-species protection, when abundant, promoted the spontaneous formation and expansion of intermixed multi-species communities that overtook or assimilated single species domains. These findings suggest that drug attenuation is a widespread phenomenon that can be key to the coexistence of antibiotic producing and sensitive microbes in close proximity and thereby to the overall species diversity within soil microenvironments. [Preview Abstract] |
Wednesday, March 5, 2014 4:54PM - 5:06PM |
Q10.00009: Population Genetics of Three Dimensional Range Expansions Maxim Lavrentovich, David Nelson We develop a simple model of genetic diversity in growing spherical cell clusters, where the growth is confined to the cluster surface. This kind of growth occurs in cells growing in soft agar, and can also serve as a simple model of avascular tumors. Mutation-selection balance in these radial expansions is strongly influenced by scaling near a neutral, voter model critical point and by the inflating frontier. We develop a scaling theory to describe how the dynamics of mutation-selection balance is cut off by inflation. Genetic drift, i.e., local fluctuations in the genetic diversity, also plays an important role, and can lead to the extinction even of selectively advantageous strains. We calculate this extinction probability, taking into account the effect of rough population frontiers. [Preview Abstract] |
Wednesday, March 5, 2014 5:06PM - 5:18PM |
Q10.00010: Coevolution of CRISPR bacteria and phage in 2 dimensions Pu Han, Michael Deem CRISPR (cluster regularly interspaced short palindromic repeats) is a newly discovered adaptive, heritable immune system of prokaryotes. It can prevent infection of prokaryotes by phage. Most bacteria and almost all archae have CRISPR. The CRISPR system incorporates short nucleotide sequences from viruses. These incorporated sequences provide a historical record of the host and predator coevolution. We simulate the coevolution of bacteria and phage in 2 dimensions. Each phage has multiple proto-spacers that the bacteria can incorporate. Each bacterium can store multiple spacers in its CRISPR. Phages can escape recognition by the CRISPR system via point mutation or recombination. We will discuss the different evolutionary consequences of point mutation or recombination on the coevolution of bacteria and phage. We will also discuss an intriguing ``dynamic phase transition'' in the number of phage as a function of time and mutation rate. We will show that due to the arm race between phages and bacteria, the frequency of spacers and proto-spacers in a population can oscillate quite rapidly. [Preview Abstract] |
Wednesday, March 5, 2014 5:18PM - 5:30PM |
Q10.00011: Genotype to Phenotype Mapping of the E. coli lac Promoter Jakub Otwinowski, Ilya Nemenman Genotype-to-phenotype maps and the related fitness landscapes that include epistatic interactions are difficult to measure because of their high dimensional structure. Here we construct such a map using the recently collected corpora of high-throughput sequence data from the 75 base pairs long mutagenized E. coli lac promoter region, where each sequence is associated with induced transcriptional activity measured by a fluorescent reporter. We find that the additive (non-epistatic) contributions of individual mutations account for about two-thirds of the explainable phenotype variance, while pairwise epistasis explains about 7\% of the variance for the full mutagenized sequence and about 15\% for the subsequence associated with protein binding sites. Surprisingly, there is no evidence for third order epistatic contributions, and our inferred fitness landscape is essentially single peaked, with a small amount of antagonistic epistasis. We identify transcription factor (CRP) and RNA polymerase binding sites in the promotor region and their interactions. We conclude with a cautionary note that inferred properties of fitness landscapes may be severely influenced by biases in the sequence data. [Preview Abstract] |
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