EVOLUTION WITH ENDOGENOUS MUTATIONS

2005 ◽  
Vol 07 (02) ◽  
pp. 229-240 ◽  
Author(s):  
IVAR KOLSTAD

Bergin and Lipman (1996) prove that equilibrium selection in the evolutionary dynamics of Kandori et al. (1993) and Young (1993), is not robust to variations in mutation rates across states. Specifically, a risk dominant equilibrium can be selected against if mutation rates are higher in its basin of attraction than elsewhere. Van Damme and Weibull (1998) model mutations as a compromise between payoff losses and control costs, which implies lower mutation rates in the risk dominant equilibrium. This paper argues that this result is not driven by control costs, but by players focusing on payoff losses when choosing mutation rates.

2000 ◽  
Vol 4 (3) ◽  
pp. 373-414 ◽  
Author(s):  
Jasmina Arifovic

This paper provides a survey of the applications of evolutionary algorithms in macroeconomic models. Discussion is organized around the issues related to stability of equilibria, equilibrium selection, transitional dynamics, and the long-run evolutionary dynamics different from rational-expectations equilibrium outcomes. The survey also discusses criteria that can be used to evaluate the performance and usefulness of evolutionary algorithms in the macroeconomic context.


2014 ◽  
Vol 4 (4) ◽  
pp. 20140037 ◽  
Author(s):  
David Liao ◽  
Thea D. Tlsty

Failure to understand evolutionary dynamics has been hypothesized as limiting our ability to control biological systems. An increasing awareness of similarities between macroscopic ecosystems and cellular tissues has inspired optimism that game theory will provide insights into the progression and control of cancer. To realize this potential, the ability to compare game theoretic models and experimental measurements of population dynamics should be broadly disseminated. In this tutorial, we present an analysis method that can be used to train parameters in game theoretic dynamics equations, used to validate the resulting equations, and used to make predictions to challenge these equations and to design treatment strategies. The data analysis techniques in this tutorial are adapted from the analysis of reaction kinetics using the method of initial rates taught in undergraduate general chemistry courses. Reliance on computer programming is avoided to encourage the adoption of these methods as routine bench activities.


Genetics ◽  
1973 ◽  
Vol 75 (1) ◽  
pp. 93-111
Author(s):  
Seaward A Sand ◽  
Harold H Smith

ABSTRACT Somatic effects of radiation intensity on the mutable V and stable R genes were detected in plants of a heterozygous clone (vS3/vs, R/r) subjected to the same dose at four rates. The effects were compared by counting speckled and purple sectors in flowers from irradiated and control plants. Response curves were estimated from the mutant sector averages, observed over a period of transient response for successive mature flowers. A structure for integrating the mutational contributions from different flowers was provided by models. The average control mutation rates are 8,110 per 107 cells for the V gene, and 49.45 for R. At a constant intensity of 4320 roentgens/hour, average induced mutation rates per 107 cells per roentgen for V increase from 194 (at 24 r total dose) to 1,116 (at 3 r dose); the corresponding rates for R increase from 7.24 to 27.65. With these responses as standards, both genes at corresponding total doses yield lower rates at lower intensities. For the series of intensities 1.2, 0.6, 0.3 and 0.15 roentgens/hour, the decreases in mutation rate for the V gene are, respectively, 66, 148, 315, and 617 per 107 cells per roentgen. The corresponding decrements for R are 4.86, 8.70, 14.61, and 23.51. These effects are non-linear functions of intensity for both genes, but V is at least 13 times as sensitive as R. Radiation operating to extinguish a buffering system against final mutation can account for the dose and dose-rate effects observed.


2021 ◽  
Author(s):  
Yoav Ram ◽  
Yitzhak Tzachi Pilpel ◽  
Gabriela Aleksandra Lobinska

The mutation rate is an important determinant of evolutionary dynamics. Because the mutation rate determines the rate of appearance of beneficial and deleterious mutations, it is subject to second-order selection. The mutation rate varies between and within species and populations, increases under stress, and is genetically controlled by mutator alleles. The mutation rate may also vary among genetically identical individuals: empirical evidence from bacteria suggests that the mutation rate may be affected by translation errors and expression noise in various proteins (1). Importantly, this non-genetic variation may be heritable via transgenerational epigenetic inheritance. Here we investigate how the inheritance mode of the mutation rate affects the rate of adaptive evolution on rugged fitness landscapes. We model an asexual population with two mutation rate phenotypes, non-mutator and mutator. An offspring may switch from its parental phenotype to the other phenotype. The rate of switching between the mutation rate phenotypes is allowed to span a range of values. Thus, the mutation rate can be interpreted as a genetically inherited trait when the switching rate is low, as an epigenetically inherited trait when the switching rate is intermediate, or as a randomly determined trait when the switching rate is high. We find that epigenetically inherited mutation rates result in the highest rates of adaptation on rugged fitness landscapes for most realistic parameter sets. This is because an intermediate switching rate can maintain the association between a mutator phenotype and pre-existing mutations, which facilitates the crossing of fitness valleys. Our results provide a rationale for the evolution of epigenetic inheritance of the mutation rate, suggesting that it could have been selected because it facilitates adaptive evolution.


2021 ◽  
Author(s):  
Manuel A. Rendón

Quadrotor control is an exciting research area. Despite last years developments, some aspects demand a deeper analysis: How a quadrotor operates in challenging trajectories, how to define trajectory limits, or how changing physical characteristics of the device affects the performance. A visual interface development platform is a valuable tool to support this effort, and one of these tools is briefly described in this Chapter. The quadrotor model uses Newton-Euler equations with Euler angles, and considers the effect of air drag and propellers’ speed dynamics, as well as measurement noise and limits for propeller speeds. The tool is able to test any device just by setting a few parameters. A three-dimensional optimal trajectory defined by a set of waypoints and corresponding times, is calculated with the help of a Minimum Snap Trajectory planning algorithm. Small Angle Control, Desired Thrust Vector (DTV) Control and Geometric Tracking Control are the available strategies in the tool for quadrotor attitude and trajectory following control. The control gains are calculated using Particle Swarm Optimization. Root Mean Square (RMS) error and Basin of Attraction are employed for validation. The tool allows to choose the control strategy by visual evaluation on a graphical user interface (GUI), or analyzing the numerical results. The tool is modular and open to other control strategies, and is available in GitHub.


PLoS Genetics ◽  
2021 ◽  
Vol 17 (11) ◽  
pp. e1009864
Author(s):  
Gemma G. R. Murray ◽  
Andrew J. Balmer ◽  
Josephine Herbert ◽  
Nazreen F. Hadijirin ◽  
Caroline L. Kemp ◽  
...  

Mutation rates vary both within and between bacterial species, and understanding what drives this variation is essential for understanding the evolutionary dynamics of bacterial populations. In this study, we investigate two factors that are predicted to influence the mutation rate: ecology and genome size. We conducted mutation accumulation experiments on eight strains of the emerging zoonotic pathogen Streptococcus suis. Natural variation within this species allows us to compare tonsil carriage and invasive disease isolates, from both more and less pathogenic populations, with a wide range of genome sizes. We find that invasive disease isolates have repeatedly evolved mutation rates that are higher than those of closely related carriage isolates, regardless of variation in genome size. Independent of this variation in overall rate, we also observe a stronger bias towards G/C to A/T mutations in isolates from more pathogenic populations, whose genomes tend to be smaller and more AT-rich. Our results suggest that ecology is a stronger correlate of mutation rate than genome size over these timescales, and that transitions to invasive disease are consistently accompanied by rapid increases in mutation rate. These results shed light on the impact that ecology can have on the adaptive potential of bacterial pathogens.


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