scholarly journals On the fixation probability of superstars

Author(s):  
Josep Díaz ◽  
Leslie Ann Goldberg ◽  
George B. Mertzios ◽  
David Richerby ◽  
Maria Serna ◽  
...  

The Moran process models the spread of genetic mutations through populations. A mutant with relative fitness r is introduced and the system evolves, either reaching fixation (an all-mutant population) or extinction (no mutants). In a widely cited paper, Lieberman et al. (2005 Evolutionary dynamics on graphs. Nature 433 , 312–316) generalize the model to populations on the vertices of graphs. They describe a class of graphs (‘superstars’), with a parameter k and state that the fixation probability tends to 1− r − k as the graphs get larger: we show that this is untrue as stated. Specifically, for k =5, we show that the fixation probability (in the limit, as graphs get larger) cannot exceed 1−1/ j ( r ), where j ( r )= Θ ( r 4 ), contrary to the claimed result. Our proof is fully rigorous, though we use a computer algebra package to invert a 31×31 symbolic matrix. We do believe the qualitative claim of Lieberman et al. —that superstar fixation probability tends to 1 as k increases—and that it can probably be proved similarly to their sketch. We were able to run larger simulations than the ones they presented. Simulations on graphs of around 40 000 vertices do not support their claim but these graphs might be too small to exhibit the limiting behaviour.

2018 ◽  
Author(s):  
David Hathcock ◽  
Steven H. Strogatz

Evolutionary graph theory models the effects of natural selection and random drift on structured populations of mutant and non-mutant individuals. Recent studies have shown that fixation times, which determine the rate of evolution, often have right-skewed distributions. Little is known, however, about how these distributions and their skew depend on mutant fitness. Here we calculate the fitness dependence of the fixation-time distribution for the Moran Birth-death process in populations modeled by two extreme networks: the complete graph and the one-dimensional ring lattice, each of which admits an exact solution in the limit of large network size. We find that with non-neutral fitness, the Moran process on the ring has normally distributed fixation times, independent of the relative fitness of mutants and non-mutants. In contrast, on the complete graph, the fixation-time distribution is a weighted convolution of two Gumbel distributions, with a weight depending on the relative fitness. When fitness is neutral, however, the Moran process has a highly skewed fixation-time distribution on both the complete graph and the ring. In this sense, the case of neutral fitness is singular. Even on these simple network structures, the fixation-time distribution exhibits rich fitness dependence, with discontinuities and regions of universality. Applications of our methods to a multi-fitness Moran model, times to partial fixation, and evolution on random networks are discussed.


Author(s):  
Karan Pattni ◽  
Mark Broom ◽  
Jan Rychtář ◽  
Lara J. Silvers

Evolution in finite populations is often modelled using the classical Moran process. Over the last 10 years, this methodology has been extended to structured populations using evolutionary graph theory. An important question in any such population is whether a rare mutant has a higher or lower chance of fixating (the fixation probability) than the Moran probability, i.e. that from the original Moran model, which represents an unstructured population. As evolutionary graph theory has developed, different ways of considering the interactions between individuals through a graph and an associated matrix of weights have been considered, as have a number of important dynamics. In this paper, we revisit the original paper on evolutionary graph theory in light of these extensions to consider these developments in an integrated way. In particular, we find general criteria for when an evolutionary graph with general weights satisfies the Moran probability for the set of six common evolutionary dynamics.


Author(s):  
Dimitra Aggeli ◽  
Yuping Li ◽  
Gavin Sherlock

AbstractThe fitness effects of random mutations are contingent upon the genetic and environmental contexts in which they occur, and this contributes to the unpredictability of evolutionary outcomes at the molecular level. Despite this unpredictability, the rate of adaptation in homogeneous environments tends to decrease over evolutionary time, due to diminishing returns epistasis, causing relative fitness gains to be predictable over the long term. Here, we studied the extent of diminishing returns epistasis and the changes in the adaptive mutational spectra after yeast populations have already taken their first adaptive mutational step. We used three distinct adaptive clones that arose under identical conditions from a common ancestor, from which they diverge by a single point mutation, to found populations that we further evolved. We followed the evolutionary dynamics of these populations by lineage tracking and determined adaptive outcomes using fitness assays and whole genome sequencing. We found compelling evidence for diminishing returns: fitness gains during the 2nd step of adaptation are smaller than those of the 1st step, due to a compressed distribution of fitness effects in the 2nd step. We also found strong evidence for historical contingency at the genic level: the beneficial mutational spectra of the 2nd-step adapted genotypes differ with respect to their ancestor and to each other, despite the fact that the three founders’ 1st-step mutations provided their fitness gains due to similar phenotypic improvements. While some targets of selection in the second step are shared with those seen in the common ancestor, other targets appear to be contingent on the specific first step mutation, with more phenotypically similar founding clones having more similar adaptive mutational spectra. Finally, we found that disruptive mutations, such as nonsense and frameshift, were much more common in the first step of adaptation, contributing an additional way that both diminishing returns and historical contingency are evident during 2nd step adaptation.


2011 ◽  
Vol 92 (8) ◽  
pp. 1930-1938 ◽  
Author(s):  
Mónica Betancourt ◽  
Aurora Fraile ◽  
Fernando García-Arenal

Two groups of Cucumber mosaic virus (CMV) satellite RNAs (satRNAs), necrogenic and non-necrogenic, can be differentiated according to the symptoms they cause in tomato plants, a host in which they also differ in fitness. In most other CMV hosts these CMV-satRNA cause similar symptoms. Here, we analyse whether they differ in traits determining their relative fitness in melon plants, in which the two groups of CMV-satRNAs cause similar symptoms. For this, ten necrogenic and ten non-necrogenic field satRNA genotypes were assayed with Fny-CMV as a helper virus. Neither type of CMV-satRNA modified Fny-CMV symptoms, and both types increased Fny-CMV virulence similarly, as measured by decreases in plant biomass and lifespan. Necrogenic and non-necrogenic satRNAs differed in their ability to multiply in melon tissues; necrogenic satRNAs accumulated to higher levels both in single infection and in competition with non-necrogenic satRNAs. Indeed, multiplication of some non-necrogenic satRNAs was undetectable. Transmission between hosts by aphids was less efficient for necrogenic satRNAs as a consequence of a more severe reduction of CMV accumulation in leaves. The effect of CMV accumulation on aphid transmission was not compensated for by differences in satRNA encapsidation efficiency or transmissibility to CMV progeny. Thus, necrogenic and non-necrogenic satRNAs differ in their relative fitness in melon, and trade-offs are apparent between the within-host and between-host components of satRNA fitness. Hence, CMV-satRNAs could have different evolutionary dynamics in CMV host-plant species in which they do not differ in pathogenicity.


2016 ◽  
Author(s):  
Xiang-Yi Li ◽  
Shun Kurokawa ◽  
Stefano Giaimo ◽  
Arne Traulsen

AbstractIn this work, we study the effects of demographic structure on evolutionary dynamics, when selection acts on reproduction, survival, or both. In contrast with the previously discovered pattern that the fixation probability of a neutral mutant decreases while population becomes younger, we show that a mutant with constant selective advantage may have a maximum or a minimum of the fixation probability in populations with an intermediate fraction of young individuals. This highlights the importance of life history and demographic structure in studying evolutionary dynamics. We also illustrate the fundamental differences between selection on reproduction and on survival when age structure is present. In addition, we evaluate the relative importance of size and structure of the population in determining the fixation probability of the mutant. Our work lays the foundation for studying also density and frequency dependent effects in populations when demographic structures cannot be neglected.


2017 ◽  
Author(s):  
Philip Gerlee ◽  
Philipp M. Altrock

AbstractCancer evolution and progression are shaped by cellular interactions and Darwinian selection. Evolutionary game theory incorporates both of these principles, and has been proposed as a framework to understand tumor cell population dynamics. A cornerstone of evolutionary dynamics is the replicator equation, which describes changes in the relative abundance of different cell types, and is able to predict evolutionary equilibria. Typically, the replicator equation focuses on differences in relative fitness. We here show that this framework might not be sufficient under all circumstances, as it neglects important aspects of population growth. Standard replicator dynamics might miss critical differences in the time it takes to reach an equilibrium, as this time also depends on cellular turnover in growing but bounded populations. As the system reaches a stable manifold, the time to reach equilibrium depends on cellular death and birth rates. These rates shape the timescales, in particular in co-evolutionary dynamics of growth factor producers and free-riders. Replicator dynamics might be an appropriate framework only when birth and death rates are of similar magnitude. Otherwise, population growth effects cannot be neglected when predicting the time to reach an equilibrium, and cell type specific rates have to be accounted for explicitly.


2021 ◽  
Vol 17 (10) ◽  
pp. e1009537
Author(s):  
Mohammad Ali Dehghani ◽  
Amir Hossein Darooneh ◽  
Mohammad Kohandel

The study of evolutionary dynamics on graphs is an interesting topic for researchers in various fields of science and mathematics. In systems with finite population, different model dynamics are distinguished by their effects on two important quantities: fixation probability and fixation time. The isothermal theorem declares that the fixation probability is the same for a wide range of graphs and it only depends on the population size. This has also been proved for more complex graphs that are called complex networks. In this work, we propose a model that couples the population dynamics to the network structure and show that in this case, the isothermal theorem is being violated. In our model the death rate of a mutant depends on its number of neighbors, and neutral drift holds only in the average. We investigate the fixation probability behavior in terms of the complexity parameter, such as the scale-free exponent for the scale-free network and the rewiring probability for the small-world network.


2014 ◽  
Vol 2014 ◽  
pp. 1-5
Author(s):  
Pei-ai Zhang

Evolutionary graph theory is a nice measure to implement evolutionary dynamics on spatial structures of populations. To calculate the fixation probability is usually regarded as a Markov chain process, which is affected by the number of the individuals, the fitness of the mutant, the game strategy, and the structure of the population. However the position of the new mutant is important to its fixation probability. Here the position of the new mutant is laid emphasis on. The method is put forward to calculate the fixation probability of an evolutionary graph (EG) of single level. Then for a class of bilevel EGs, their fixation probabilities are calculated and some propositions are discussed. The conclusion is obtained showing that the bilevel EG is more stable than the corresponding one-rooted EG.


2017 ◽  
Vol 14 (134) ◽  
pp. 20170342 ◽  
Author(s):  
Philip Gerlee ◽  
Philipp M. Altrock

Cancer evolution and progression are shaped by cellular interactions and Darwinian selection. Evolutionary game theory incorporates both of these principles, and has been proposed as a framework to understand tumour cell population dynamics. A cornerstone of evolutionary dynamics is the replicator equation, which describes changes in the relative abundance of different cell types, and is able to predict evolutionary equilibria. Typically, the replicator equation focuses on differences in relative fitness. We here show that this framework might not be sufficient under all circumstances, as it neglects important aspects of population growth. Standard replicator dynamics might miss critical differences in the time it takes to reach an equilibrium, as this time also depends on cellular turnover in growing but bounded populations. As the system reaches a stable manifold, the time to reach equilibrium depends on cellular death and birth rates. These rates shape the time scales, in particular, in coevolutionary dynamics of growth factor producers and free-riders. Replicator dynamics might be an appropriate framework only when birth and death rates are of similar magnitude. Otherwise, population growth effects cannot be neglected when predicting the time to reach an equilibrium, and cell-type-specific rates have to be accounted for explicitly.


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