How altruism evolves: assortment and synergy.
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Altruism↗
Biomedical subjects
M Doebeli
Publications and source records attributed to M Doebeli.
Adaptive speciation when assortative mating is based on female preference for male marker traits.
Adaptive speciation occurs when frequency-dependent ecological interactions generate conditions of disruptive selection to which lineage splitting is an adaptive response. Under such selective conditions, evolution of assortative mating mechanisms enables the break-up of the ancestral lineage into diverging and reproductively isolated descendent species. Extending previous studies, I investigate models of adaptive speciation due to the evolution of indirect assortative mating that is based on three different mating traits: the degree of assortativity, a female preference trait and a male marker trait. For speciation to occur, linkage disequilibria between different mating traits, e.g. between female preference and male marker traits, as well as between mating traits and the ecological trait, must evolve. This can lead to novel speciation scenarios, e.g. when reproductive isolation is generated by a splitting in the degree of assortativeness, with one of the emerging lineages mating assortatively, and the other one disassortatively. I investigate the effects of variation in various model parameters on the likelihood of speciation, as well as robustness of speciation to introducing costs of assortative mating. Even though in the models presented speciation requires the genetic potential for strong assortment as well as rather restrictive ecological conditions, the results show that adaptive speciation due to the evolution of assortative mating when mate choice is based on separate female preference and male marker traits is a theoretically plausible evolutionary scenario.
Adaptation, Biological↗
Adaptive dynamics as a mathematical tool for studying the ecology of speciation processes.
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Adaptation, Biological↗
Pluralism in evolutionary theory.
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Adaptation, Biological↗
A bit of sex stabilizes host-parasite dynamics.
To date, only a few studies have focused on the effects of sex on population dynamics. Previous models have typically found that sexual reproduction dampens population fluctuations. Although asexual and sexual reproduction are just the two endpoints along a continuum of varying rates of sex, previous work has ignored the effects of intermediate degrees of sex on population dynamics. Here we study the effects of partial sexual reproduction (i.e. sex occurs only every few generations or with small probability in each generation) on the coupled population dynamics of a Nicholson-Bailey host-parasite model. We show that complex dynamics are simplified for high host population growth rates if the frequency of sex is sufficiently high in both host and parasite: sex decreases fluctuations in population density, and leads to non-chaotic dynamics for population growth rates that would result in chaotic dynamics in the absence of sexual reproduction. However, the simplification does not increase gradually with an increasing frequency of sex but appears abruptly at low-to-intermediate frequencies of sex. For some parameter settings, intermediate frequencies of sexual reproduction can simplify the dynamics more than lower or higher frequencies. Thus, in agreement with earlier results, sexual reproduction typically stabilizes complex population dynamics in our models. Additionally, our results suggest that low-to-intermediate frequencies of sex may often be as (or even more) stabilizing as high frequencies.
Animals↗
Experimental evolution of aging, growth, and reproduction in fruitflies.
We report in this paper an evolutionary experiment on Drosophila that tested life-history theory and the evolutionary theory of aging. As theory predicts, higher extrinsic mortality rates did lead to the evolution of higher intrinsic mortality rates, to shorter lifespans, and to decreased age and size at eclosion; peak fecundity also shifted earlier in life. These results confirm the key role of extrinsic mortality rates in the evolution of growth, maturation, reproduction, and aging, and they do so with a selection regime that maintained selection on fertility throughout life while holding population densities constant.
Aging↗
Evolution of cooperation in spatially structured populations
Using a spatial lattice model of the Iterated Prisoner's Dilemma we studied the evolution of cooperation within the strategy space of all stochastic strategies with a memory of one round. Comparing the spatial model with a randomly mixed model showed that (1) there is more cooperative behaviour in a spatially structured population, (2) PAVLOV and generous variants of it are very successful strategies in the spatial context and (3) in spatially structured populations evolution is much less chaotic than in unstructured populations. In spatially structured populations, generous variants of PAVLOV are found to be very successful strategies in playing the Iterated Prisoner's Dilemma. The main weakness of PAVLOV is that it is exploitable by defective strategies. In a spatial context this disadvantage is much less important than the good error correction of PAVLOV, and especially of generous PAVLOV, because in a spatially structured population successful strategies always build clusters. Copyright 1999 Academic Press.
Journal Article↗
Variable investment, the Continuous Prisoner's Dilemma, and the origin of cooperation.
Cooperation is fundamental to many biological systems. A common metaphor for studying the evolution of cooperation is the Prisoner's Dilemma, a game with two strategies: cooperate or defect. However, cooperation is rare all or nothing, and its evolution probably involves the gradual extension of initially modest degrees of assistance. The inability of the Prisoner's Dilemma to capture this basic aspect limits its use for understanding the evolutionary origins of cooperation. Here we consider a framework for cooperation based on the concept of investment: an act which is costly, but which benefits other individuals, where the cost and benefit depend on the level of investment made. In the resulting Continuous Prisoner's Dilemma the essential problem of cooperation remains: in the absence of any additional structure non-zero levels of investment cannot evolve. However, if investments are considered in a spatially structured context, selfish individuals who make arbitrarily low investments can be invaded by higher-investing mutants. This results in the mean level of investment evolving to significant levels, where it is maintained indefinitely. This approach provides a natural solution to the fundamental problem of how cooperation gradually increases from a non-cooperative state.
Biological Evolution↗
'Raise the stakes' evolves into a defector.
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Altruism↗
On the origin of species by sympatric speciation.
Understanding speciation is a fundamental biological problem. It is believed that many species originated through allopatric divergence, where new species arise from geographically isolated populations of the same ancestral species. In contrast, the possibility of sympatric speciation (in which new species arise without geographical isolation) has often been dismissed, partly because of theoretical difficulties. Most previous models analysing sympatric speciation concentrated on particular aspects of the problem while neglecting others. Here we present a model that integrates a novel combination of different features and show that sympatric speciation is a likely outcome of competition for resources. We use multilocus genetics to describe sexual reproduction in an individual-based model, and we consider the evolution of assortative mating (where individuals mate preferentially with like individuals) depending either on an ecological character affecting resource use or on a selectively neutral marker trait. In both cases, evolution of assortative mating often leads to reproductive isolation between ecologically diverging subpopulations. When assortative mating depends on a marker trait, and is therefore not directly linked to resource competition, speciation occurs when genetic drift breaks the linkage equilibrium between the marker and the ecological trait. Our theory conforms well with mounting empirical evidence for the sympatric origin of many species.
Animals↗
Population dynamics and the evolution of virulence in epidemiological models with discrete host generations
Chaos is the likely outcome of the interaction between a parasite and a host with discrete generations, if the parasite's virulence is high and if transmission from one generation to the next is held constant. We studied two alternative routes of transmission-vertical transmission from infecteds to their offspring, and transmission via long-lasting spores produced in those individuals that were killed by the infection-to investigate the influence of the transmission route on the system's evolution and population dynamics. The major results are: (1) vertical transmission often leads to low virulence, thus confirming most epidemiological models. However, if hosts can become super-infected, the evolutionary dynamics of virulence can have several equilibrium points, including 100% disease-induced mortality; (2) when parasites are transmitted with long-lasting spores, the evolutionary dynamics of virulence can become unstable, leading to the repeated bifurcation of two sub-populations with high and low virulence or to punctuated equilibria with sudden changes in the average level of virulence; (3) in general, the evolution of virulence moves the system to an area where the population dynamics are stable. When evolution leads to chaos, the system most often becomes extinct. Only for a restricted parameter space in the system where transmission from one generation to the next is via long-lasting spores do the dynamics become chaotic without extinction of the system. Copyright 1999 Academic Press.
Journal Article↗
Genetic variability in sensitivity to population density affects the dynamics of simple ecological models.
Many 1-dimensional discrete time ecological models contain a sensitivity parameter that does not affect the dynamic complexity of these models. We show that genetic variability in this parameter can have a strong effect on population dynamics. We incorporate ecological dynamics in two different population genetic models with one locus and two alleles. The first is the classical model of a randomly mating population in Hardy-Weinberg equilibrium, and the second is a model of differential selection in males and females. In populations in Hardy-Weinberg equilibrium, variability in the sensitivity parameter can be maintained by overdominance. In this case, the dynamics of the polymorphic population tend to be much simpler than those of monomorphic populations. In the model with different selection in males and females, polymorphisms can be maintained in various ways, e.g., by opposing directional selection in males and females. Polymorphism in the sensitivity parameter tends to simplify population dynamics in the model with different selection in males and females as well. A number of interesting dynamic effects can be observed, e.g., multiple attractors with complicated basins of attraction. Then the final state of the system after a successful invasion by mutant alleles may depend on the mutation rate and on the distribution of mutational steps. In addition, there are situations in which genetic variability destabilizes a stable population dynamic equilibrium in the monomorphic model. There is an analogy between genetic variability and variability imposed by the environment. If differences in sensitivity are caused by the environment, dynamic effects similar to those in the genetic models can be observed. In addition, source-sink structures that are known to occur in spatially structured models can be seen in the genetic model if one of the genotypes is inviable. The results suggest that combining ecological and population genetic models can lead to a number of new insights. More work is needed, e.g., with fertility models, in which fitnesses are not assigned to individuals, but to mating pairs.
Alleles↗
The evolution of interspecific mutualisms.
Interspecific mutualisms are widespread, but how they evolve is not clear. The Iterated Prisoner's Dilemma is the main theoretical tool to study cooperation, but this model ignores ecological differences between partners and assumes that amounts exchanged cannot themselves evolve. A more realistic model incorporating these features shows that strategies that succeed with fixed exchanges (e. g., Tit-for-Tat) cannot explain mutualism when exchanges vary because the amount exchanged evolves to 0. For mutualism to evolve, increased investments in a partner must yield increased returns, and spatial structure in competitive interactions is required. Under these biologically plausible assumptions, mutualism evolves with surprising ease. This suggests that, contrary to the basic premise of past theoretical analyses, overcoming a potential host's initial defenses may be a bigger obstacle for mutualism than the subsequent recurrence and spread of noncooperative mutants.
Biological Evolution↗
Self-organized criticality in spatial evolutionary game theory.
Self-organized criticality is an important framework for understanding the emergence of scale-free natural phenomena. Cellular automata provide simple interesting models in which to study self-organized criticality. We consider the dynamics of a new class of cellular automata which are constructed as natural spatial extensions of evolutionary game theory. This construction yields a discrete one-parameter family of cellular automata. We show that there is a range of parameter values for which this system exhibits complex dynamics with long range correlations between states in both time and space. In this region the dynamics evolve to a self-organized critical state in which structures exist on all time and length scales, and the relevant statistical measures have power law behaviour.
Animals↗
Population dynamics, demographic stochasticity, and the evolution of cooperation.
A basic evolutionary problem posed by the Iterated Prisoner's Dilemma game is to understand when the paradigmatic cooperative strategy Tit-for-Tat can invade a population of pure defectors. Deterministically, this is impossible. We consider the role of demographic stochasticity by embedding the Iterated Prisoner's Dilemma into a population dynamic framework. Tit-for-Tat can invade a population of defectors when their dynamics exhibit short episodes of high population densities with subsequent crashes and long low density periods with strong genetic drift. Such dynamics tend to have reddened power spectra and temporal distributions of population size that are asymmetric and skewed toward low densities. The results indicate that ecological dynamics are important for evolutionary shifts between adaptive peaks.
Biological Evolution↗
High molecular weight forms of IGF-II ('big-IGF-II') released by Wilms' tumor cells.
Insulin-like growth factor-II (IGF-II) is thought to play a critical role in the development of embryonic tumors such as Wilms' tumor. However, despite highly elevated IGF-II mRNA levels in tumors, IGF-II is not elevated in the serum of patients with Wilms' tumors. Recently high molecular weight forms of IGF-II ('big'- or pro-IGF-II) have been found to be produced by some tumors. In order to prove whether or not high molecular weight forms of IGF-II are produced by Wilms' tumor cells and secreted into the culture medium, we established Wilms' tumor cell lines. After column chromatography of the culture medium, IGF-II and pro-IGF-II concentrations were measured. For pro-IGF-II measurement we established a pro-IGF-II RIA using a rabbit polyclonal antiserum directed against amino acids 7-21 (E7-21) of the E-domain of pro-IGF-II. Gel electrophoresis and Western blotting with anti-IGF-II antibodies revealed a band at 7.5 kDa corresponding to fully processed IGF-II and bands between 10 and 20 kDa. Using pro-IGF-II antiserum, bands between 10 and 25 kDa were detected. We conclude that in vitro cultured Wilms' tumor cells produce and release various forms of 'big IGF-II' with molecular masses between 10 and 25 kDa. It remains uncertain whether these high molecular weight forms of IGF-II represent normal precursors of IGF-II or incorrectly processed IGF-II.
Animals↗