@article{696,
abstract = {Mutator strains are expected to evolve when the availability and effect of beneficial mutations are high enough to counteract the disadvantage from deleterious mutations that will inevitably accumulate. As the population becomes more adapted to its environment, both availability and effect of beneficial mutations necessarily decrease and mutation rates are predicted to decrease. It has been shown that certain molecular mechanisms can lead to increased mutation rates when the organism finds itself in a stressful environment. While this may be a correlated response to other functions, it could also be an adaptive mechanism, raising mutation rates only when it is most advantageous. Here, we use a mathematical model to investigate the plausibility of the adaptive hypothesis. We show that such a mechanism can be mantained if the population is subjected to diverse stresses. By simulating various antibiotic treatment schemes, we find that combination treatments can reduce the effectiveness of second-order selection on stress-induced mutagenesis. We discuss the implications of our results to strategies of antibiotic therapy.},
author = {Lukacisinova, Marta and Novak, Sebastian and Paixao, Tiago},
issn = {1553734X},
journal = {PLoS Computational Biology},
number = {7},
publisher = {Public Library of Science},
title = {{Stress induced mutagenesis: Stress diversity facilitates the persistence of mutator genes}},
doi = {10.1371/journal.pcbi.1005609},
volume = {13},
year = {2017},
}
@article{910,
abstract = {Frequency-independent selection is generally considered as a force that acts to reduce the genetic variation in evolving populations, yet rigorous arguments for this idea are scarce. When selection fluctuates in time, it is unclear whether frequency-independent selection may maintain genetic polymorphism without invoking additional mechanisms. We show that constant frequency-independent selection with arbitrary epistasis on a well-mixed haploid population eliminates genetic variation if we assume linkage equilibrium between alleles. To this end, we introduce the notion of frequency-independent selection at the level of alleles, which is sufficient to prove our claim and contains the notion of frequency-independent selection on haploids. When selection and recombination are weak but of the same order, there may be strong linkage disequilibrium; numerical calculations show that stable equilibria are highly unlikely. Using the example of a diallelic two-locus model, we then demonstrate that frequency-independent selection that fluctuates in time can maintain stable polymorphism if linkage disequilibrium changes its sign periodically. We put our findings in the context of results from the existing literature and point out those scenarios in which the possible role of frequency-independent selection in maintaining genetic variation remains unclear.
},
author = {Novak, Sebastian and Barton, Nicholas H},
journal = {Genetics},
number = {2},
pages = {653 -- 668},
publisher = {Genetics Society of America},
title = {{When does frequency-independent selection maintain genetic variation?}},
doi = {10.1534/genetics.117.300129},
volume = {207},
year = {2017},
}
@article{1191,
abstract = {Variation in genotypes may be responsible for differences in dispersal rates, directional biases, and growth rates of individuals. These traits may favor certain genotypes and enhance their spatiotemporal spreading into areas occupied by the less advantageous genotypes. We study how these factors influence the speed of spreading in the case of two competing genotypes under the assumption that spatial variation of the total population is small compared to the spatial variation of the frequencies of the genotypes in the population. In that case, the dynamics of the frequency of one of the genotypes is approximately described by a generalized Fisher–Kolmogorov–Petrovskii–Piskunov (F–KPP) equation. This generalized F–KPP equation with (nonlinear) frequency-dependent diffusion and advection terms admits traveling wave solutions that characterize the invasion of the dominant genotype. Our existence results generalize the classical theory for traveling waves for the F–KPP with constant coefficients. Moreover, in the particular case of the quadratic (monostable) nonlinear growth–decay rate in the generalized F–KPP we study in detail the influence of the variance in diffusion and mean displacement rates of the two genotypes on the minimal wave propagation speed.},
author = {Kollár, Richard and Novak, Sebastian},
journal = {Bulletin of Mathematical Biology},
number = {3},
pages = {525--559},
publisher = {Springer},
title = {{Existence of traveling waves for the generalized F–KPP equation}},
doi = {10.1007/s11538-016-0244-3},
volume = {79},
year = {2017},
}
@article{1169,
abstract = {Dispersal is a crucial factor in natural evolution, since it determines the habitat experienced by any population and defines the spatial scale of interactions between individuals. There is compelling evidence for systematic differences in dispersal characteristics within the same population, i.e., genotype-dependent dispersal. The consequences of genotype-dependent dispersal on other evolutionary phenomena, however, are poorly understood. In this article we investigate the effect of genotype-dependent dispersal on spatial gene frequency patterns, using a generalization of the classical diffusion model of selection and dispersal. Dispersal is characterized by the variance of dispersal (diffusion coefficient) and the mean displacement (directional advection term). We demonstrate that genotype-dependent dispersal may change the qualitative behavior of Fisher waves, which change from being “pulled” to being “pushed” wave fronts as the discrepancy in dispersal between genotypes increases. The speed of any wave is partitioned into components due to selection, genotype-dependent variance of dispersal, and genotype-dependent mean displacement. We apply our findings to wave fronts maintained by selection against heterozygotes. Furthermore, we identify a benefit of increased variance of dispersal, quantify its effect on the speed of the wave, and discuss the implications for the evolution of dispersal strategies.},
author = {Novak, Sebastian and Kollár, Richard},
issn = {00166731},
journal = {Genetics},
number = {1},
pages = {367 -- 374},
publisher = {Genetics Society of America},
title = {{Spatial gene frequency waves under genotype dependent dispersal}},
doi = {10.1534/genetics.116.193946},
volume = {205},
year = {2017},
}
@phdthesis{1125,
abstract = {Natural environments are never constant but subject to spatial and temporal change on
all scales, increasingly so due to human activity. Hence, it is crucial to understand the
impact of environmental variation on evolutionary processes. In this thesis, I present
three topics that share the common theme of environmental variation, yet illustrate its
effect from different perspectives.
First, I show how a temporally fluctuating environment gives rise to second-order
selection on a modifier for stress-induced mutagenesis. Without fluctuations, when
populations are adapted to their environment, mutation rates are minimized. I argue
that a stress-induced mutator mechanism may only be maintained if the population is
repeatedly subjected to diverse environmental challenges, and I outline implications of
the presented results to antibiotic treatment strategies.
Second, I discuss my work on the evolution of dispersal. Besides reproducing
known results about the effect of heterogeneous habitats on dispersal, it identifies
spatial changes in dispersal type frequencies as a source for selection for increased
propensities to disperse. This concept contains effects of relatedness that are known
to promote dispersal, and I explain how it identifies other forces selecting for dispersal
and puts them on a common scale.
Third, I analyse genetic variances of phenotypic traits under multivariate stabilizing
selection. For the case of constant environments, I generalize known formulae of
equilibrium variances to multiple traits and discuss how the genetic variance of a focal
trait is influenced by selection on background traits. I conclude by presenting ideas and
preliminary work aiming at including environmental fluctuations in the form of moving
trait optima into the model.},
author = {Novak, Sebastian},
pages = {124},
publisher = {IST Austria},
title = {{Evolutionary proccesses in variable emvironments}},
year = {2016},
}
@article{1809,
abstract = {Background: Indirect genetic effects (IGEs) occur when genes expressed in one individual alter the expression of traits in social partners. Previous studies focused on the evolutionary consequences and evolutionary dynamics of IGEs, using equilibrium solutions to predict phenotypes in subsequent generations. However, whether or not such steady states may be reached may depend on the dynamics of interactions themselves. Results: In our study, we focus on the dynamics of social interactions and indirect genetic effects and investigate how they modify phenotypes over time. Unlike previous IGE studies, we do not analyse evolutionary dynamics; rather we consider within-individual phenotypic changes, also referred to as phenotypic plasticity. We analyse iterative interactions, when individuals interact in a series of discontinuous events, and investigate the stability of steady state solutions and the dependence on model parameters, such as population size, strength, and the nature of interactions. We show that for interactions where a feedback loop occurs, the possible parameter space of interaction strength is fairly limited, affecting the evolutionary consequences of IGEs. We discuss the implications of our results for current IGE model predictions and their limitations.},
author = {Trubenova, Barbora and Novak, Sebastian and Hager, Reinmar},
journal = {PLoS One},
number = {5},
publisher = {Public Library of Science},
title = {{Indirect genetic effects and the dynamics of social interactions}},
doi = {10.1371/journal.pone.0126907},
volume = {10},
year = {2015},
}
@article{1850,
abstract = {Entomopathogenic fungi are potent biocontrol agents that are widely used against insect pests, many of which are social insects. Nevertheless, theoretical investigations of their particular life history are scarce. We develop a model that takes into account the main distinguishing features between traditionally studied diseases and obligate killing pathogens, like the (biocontrol-relevant) insect-pathogenic fungi Metarhizium and Beauveria. First, obligate killing entomopathogenic fungi produce new infectious particles (conidiospores) only after host death and not yet on the living host. Second, the killing rates of entomopathogenic fungi depend strongly on the initial exposure dosage, thus we explicitly consider the pathogen load of individual hosts. Further, we make the model applicable not only to solitary host species, but also to group living species by incorporating social interactions between hosts, like the collective disease defences of insect societies. Our results identify the optimal killing rate for the pathogen that minimises its invasion threshold. Furthermore, we find that the rate of contact between hosts has an ambivalent effect: dense interaction networks between individuals are considered to facilitate disease outbreaks because of increased pathogen transmission. In social insects, this is compensated by their collective disease defences, i.e., social immunity. For the type of pathogens considered here, we show that even without social immunity, high contact rates between live individuals dilute the pathogen in the host colony and hence can reduce individual pathogen loads below disease-causing levels.},
author = {Novak, Sebastian and Cremer, Sylvia},
journal = {Journal of Theoretical Biology},
number = {5},
pages = {54 -- 64},
publisher = {Elsevier},
title = {{Fungal disease dynamics in insect societies: Optimal killing rates and the ambivalent effect of high social interaction rates}},
doi = {10.1016/j.jtbi.2015.02.018},
volume = {372},
year = {2015},
}
@article{2023,
abstract = {Understanding the evolution of dispersal is essential for understanding and predicting the dynamics of natural populations. Two main factors are known to influence dispersal evolution: spatio-temporal variation in the environment and relatedness between individuals. However, the relation between these factors is still poorly understood, and they are usually treated separately. In this article, I present a theoretical framework that contains and connects effects of both environmental variation and relatedness, and reproduces and extends their known features. Spatial habitat variation selects for balanced dispersal strategies, whereby the population is kept at an ideal free distribution. Within this class of dispersal strategies, I explain how increased dispersal is promoted by perturbations to the dispersal type frequencies. An explicit formula shows the magnitude of the selective advantage of increased dispersal in terms of the spatial variability in the frequencies of the different dispersal strategies present. These variances are capable of capturing various sources of stochasticity and hence establish a common scale for their effects on the evolution of dispersal. The results furthermore indicate an alternative approach to identifying effects of relatedness on dispersal evolution.},
author = {Novak, Sebastian},
journal = {Ecology and Evolution},
number = {24},
pages = {4589 -- 4597},
publisher = {Wiley-Blackwell},
title = {{Habitat heterogeneities versus spatial type frequency variances as driving forces of dispersal evolution}},
doi = {10.1002/ece3.1289},
volume = {4},
year = {2014},
}
@article{2169,
author = {Barton, Nicholas H and Novak, Sebastian and Paixao, Tiago},
journal = {PNAS},
number = {29},
pages = {10398 -- 10399},
publisher = {National Academy of Sciences},
title = {{Diverse forms of selection in evolution and computer science}},
doi = {10.1073/pnas.1410107111},
volume = {111},
year = {2014},
}
@article{2817,
abstract = {The basic idea of evolutionary game theory is that payoff determines reproductive rate. Successful individuals have a higher payoff and produce more offspring. But in evolutionary and ecological situations there is not only reproductive rate but also carrying capacity. Individuals may differ in their exposure to density limiting effects. Here we explore an alternative approach to evolutionary game theory by assuming that the payoff from the game determines the carrying capacity of individual phenotypes. Successful strategies are less affected by density limitation (crowding) and reach higher equilibrium abundance. We demonstrate similarities and differences between our framework and the standard replicator equation. Our equation is defined on the positive orthant, instead of the simplex, but has the same equilibrium points as the replicator equation. Linear stability analysis produces the classical conditions for asymptotic stability of pure strategies, but the stability properties of internal equilibria can differ in the two frameworks. For example, in a two-strategy game with an internal equilibrium that is always stable under the replicator equation, the corresponding equilibrium can be unstable in the new framework resulting in a limit cycle.},
author = {Novak, Sebastian and Chatterjee, Krishnendu and Nowak, Martin},
journal = {Journal of Theoretical Biology},
pages = {26 -- 34},
publisher = {Elsevier},
title = {{Density games}},
doi = {10.1016/j.jtbi.2013.05.029},
volume = {334},
year = {2013},
}
@article{1863,
abstract = {The Levene model is the simplest mathematical model to describe the evolution of gene frequencies in spatially subdivided populations. It provides insight into how locally varying selection promotes a population’s genetic diversity. Despite its simplicity, interesting problems have remained unsolved even in the diallelic case. In this paper we answer an open problem by establishing that for two alleles at one locus and J demes, up to 2J−1 polymorphic equilibria may coexist. We first present a proof for the case of stable monomorphisms and then show that the result also holds for protected alleles. These findings allow us to prove that any odd number (up to 2J−1) of equilibria is possible, before we extend the proof to even numbers. We conclude with some numerical results and show that for J>2, the proportion of parameter space affording this maximum is extremely small.},
author = {Sebastian Novak},
journal = {Theoretical Population Biology},
number = {3},
pages = {97 -- 101},
publisher = {Academic Press},
title = {{The number of equilibria in the diallelic Levene model with multiple demes}},
doi = {10.1016/j.tpb.2010.12.002},
volume = {79},
year = {2011},
}