Multiple scales in metapopulations of public goods producers

Bauer, Marianne; Frey, Erwin

doi:10.1103/physreve.97.042307

Cited by 20 publications

(23 citation statements)

References 77 publications

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“…It will also be critical to evaluate the extent to which spatial interactions modify strategy-environment feedback in proposed generalizations [15] of the replicator framework underlying the present work [4] and in stochastic games with feedback between behavior and public good states [16]. Finally, the spatial approach may also aid efforts to understand how microorganisms produce and utilize public goods, e.g., siderophores -extracellular iron harvesting enzymes [6,[17][18][19][20]. Given increasing pressures on limited resources, we intend to leverage prior work on controlling mean-field strategy-environment dynamics [21] to identify ways in which local manipulation of resources, strategies, and/or perceptions can help stabilize and conserve the commons.…”

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confidence: 99%

Spatial Interactions and Oscillatory Tragedies of the Commons

Yu-hui

Weitz

2019

Phys. Rev. Lett.

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A tragedy of the commons (TOC) occurs when individuals acting in their own self-interest deplete commonly-held resources, leading to a worse outcome than had they cooperated. Over time, the depletion of resources can change incentives for subsequent actions. Here, we investigate longterm feedback between game and environment across a continuum of incentives in an individualbased framework. We identify payoff-dependent transition rules that lead to oscillatory TOC-s in stochastic simulations and the mean field limit. Further extending the stochastic model, we find that spatially explicit interactions can lead to emergent, localized dynamics, including the propagation of cooperative wave fronts and cluster formation of both social context and resources. These dynamics suggest new mechanisms underlying how TOCs arise and how they might be averted.

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confidence: 99%

Spatial Interactions and Oscillatory Tragedies of the Commons

Yu-hui

Weitz

2019

Phys. Rev. Lett.

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“…The public goods game has been extensively used in the context of human societies, and the concepts have been applied to other systems, such as microbial colonies, and insect communities (Hofbauer & Sigmund 1998, Hauert et al 2006, Nowak 2006, Allen et al 2013, Nanda & Durrett 2017, Bauer & Frey 2018. In this model, both the producer and non-producer benefit from the products produced solely by the former (see Fig.…”

Section: Resultsmentioning

confidence: 99%

Share, but unequally: A mechanism for emergence and maintenance of intratumor heterogeneity

Thirumalai

2018

Preprint

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Intratumor heterogeneity (ITH), referring to coexistence of different cell subpopulations in a single tumor, has been a major puzzle in cancer research for almost half a century. The lack of understanding of the underlying mechanism of ITH hinders progress in developing effective therapies for cancers. Based on the findings in a recent quantitative experiment on pancreatic cancer we developed a general evolutionary model, accounting for interactions between different cell populations through paracrine or juxtacrine factors. We show that the emergence of a stable heterogeneous state in a tumor requires an unequal allocation of paracrine growth factors ("public goods") between cells that produce them and those that merely consume them. Our model provides a quantitative explanation of recent in vitro experimental studies in pancreatic cancer in which insulin growth factor (IGF-II) plays the role of public goods. The calculated phase diagrams as a function of exogenous resources and fraction of growth factor producing cells show ITH persists only in a narrow range of concentration of exogenous IGF-II. Remarkably, maintenance of ITH requires cooperation among tumor cell subpopulations in harsh conditions, specified by lack of exogenous IGF-II, whereas surplus exogenous IGF-II elicits competition. The theory also quantitatively accounts for measured in vivo tumor growth in glioblastoma multiforme (GBM). The predictions for GBM tumor growth as a function of the fraction of tumor cells are amenable to experimental tests. The mechanism for ITH also provides hints for devising efficacious therapies. *

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“…Phenotypic delay may also affect other processes. For example, it was recently shown that a delay in evolutionary adaptation can lead to coexistence of spatial populations, in cases where immediate adaptation would eradicate coexistence [91,92]. A delay in evolutionary adaptation has also been postulated to explain the effect of antibiotic pulses of different lengths on the probability of resistance emerging [93].…”

Section: Discussionmentioning

confidence: 99%

Phenotypic delay in the evolution of bacterial antibiotic resistance: mechanistic models and their implications

Carballo-Pacheco

Nicholson

Lilja

et al. 2019

Preprint

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Phenotypic delay -the time delay between genetic mutation and expression of the corresponding phenotype -is generally neglected in evolutionary models, yet recent work suggests that it may be more common than previously assumed. Here, we use computer simulations and theory to investigate the significance of phenotypic delay for the evolution of bacterial resistance to antibiotics. We consider three mechanisms which could potentially cause phenotypic delay: effective polyploidy, dilution of antibiotic-sensitive molecules and accumulation of resistance-enhancing molecules. We find that the accumulation of resistant molecules is relevant only within a narrow parameter range, but both the dilution of sensitive molecules and effective polyploidy can cause phenotypic delay over a wide range of parameters. We further investigate whether these mechanisms could affect population survival under drug treatment and thereby explain observed discrepancies in mutation rates estimated by Luria-Delbrück fluctuation tests. While the effective polyploidy mechanism does not affect population survival, the dilution of sensitive molecules leads both to decreased probability of survival under drug treatment and underestimation of mutation rates in fluctuation tests. The dilution mechanism also changes the shape of the Luria-Delbrück distribution of mutant numbers, and we show that this modified distribution provides an improved fit to previously published experimental data. Author SummaryUnderstanding precisely how some bacteria survive exposure to antibiotics is a major research focus. Specific mutations in the bacterial genome are known to provide protection. However, it remains unclear how much time passes between a bacterium acquiring the genetic change and being able to tolerate antibiotics -termed the phenotypic delay -and what controls this delay. Here, using computer simulations and mathematical arguments we discuss three biologically plausible mechanisms of phenotypic delay. We investigate how each mechanism would affect the outcome of laboratory experiments often used to study the evolution of antibiotic resistance, and we highlight ¶These authors contributed equally to this work. *Corresponding authors: rosalind.allen@ed.ac.uk, bwaclaw@staffmail.ed.ac.uk 1 how the delay might be detected in such experiments. We also show that the existence of the delay could explain an observed discrepancy in the measurement of mutation rates, and demonstrate that one of our models provides a superior fit to experimental data. Our work exposes how molecular details at the intracellular level can have a direct effect on evolution at the population level.

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Multiple scales in metapopulations of public goods producers

Cited by 20 publications

References 77 publications

Spatial Interactions and Oscillatory Tragedies of the Commons

Spatial Interactions and Oscillatory Tragedies of the Commons

Share, but unequally: A mechanism for emergence and maintenance of intratumor heterogeneity

Phenotypic delay in the evolution of bacterial antibiotic resistance: mechanistic models and their implications

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