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Santos M.,Autonomous University of Barcelona | Szathmary E.,Parmenides Center for the Conceptual Foundations of Science | Szathmary E.,Eotvos Lorand University | Szathmary E.,Ludwig Maximilians University of Munich | Fontanari J.F.,University of Sao Paulo
Journal of Theoretical Biology | Year: 2015

An increasing number of dissident voices claim that the standard neo-Darwinian view of genes as 'leaders' and phenotypes as 'followers' during the process of adaptive evolution should be turned on its head. This idea is older than the rediscovery of Mendel's laws of inheritance, with the turn-of-the-twentieth-century notion eventually labeled as the 'Baldwin effect' as one of the many ways in which the standard neo-Darwinian view can be turned around. A condition for this effect is that environmentally induced variation such as phenotypic plasticity or learning is crucial for the initial establishment of a trait. This gives the additional time for natural selection to act on genetic variation and the adaptive trait can be eventually encoded in the genotype. An influential paper published in the late 1980s claimed the Baldwin effect to happen in computer simulations, and avowed that it was crucial to solve a difficult adaptive task. This generated much excitement among scholars in various disciplines that regard neo-Darwinian accounts to explain the evolutionary emergence of high-order phenotypic traits such as consciousness or language almost hopeless. Here, we use analytical and computational approaches to show that a standard population genetics treatment can easily crack what the scientific community has granted as an unsolvable adaptive problem without learning. Evolutionary psychologists and linguists have invoked the (claimed) Baldwin effect to make wild assertions that should not be taken seriously. What the Baldwin effect needs are plausible case-histories. © 2015 Elsevier Ltd.

Kun A.,International Institute For Applied Systems Analysis | Kun A.,Parmenides Center for the Conceptual Foundations of Science | Kun A.,Eotvos Lorand University | Kun A.,Hungarian Academy of Sciences | Dieckmann U.,International Institute For Applied Systems Analysis
Nature Communications | Year: 2013

Although social structure is known to promote cooperation, by locally exposing selfish agents to their own deeds, studies to date assumed that all agents have access to the same level of resources. This is clearly unrealistic. Here we find that cooperation can be maintained when some agents have access to more resources than others. Cooperation can then emerge even in populations in which the temptation to defect is so strong that players would act fully selfishly if their resources were distributed uniformly. Resource heterogeneity can thus be crucial for the emergence and maintenance of cooperation. We also show that resource heterogeneity can hinder cooperation once the temptation to defect is significantly lowered. In all cases, the level of cooperation can be maximized by managing resource heterogeneity. © 2013 Macmillan Publishers Limited. All rights reserved.

Konnyu B.,Eotvos Lorand University | Szilagyi A.,MTA ELTE Theoretical Biology and Evolutionary Ecology Research Group | Szilagyi A.,Parmenides Center for the Conceptual Foundations of Science | Czaran T.,MTA ELTE Theoretical Biology and Evolutionary Ecology Research Group
Biology Direct | Year: 2015

Background: The RNA World hypothesis offers a plausible bridge from no-life to life on prebiotic Earth, by assuming that RNA, the only known molecule type capable of playing genetic and catalytic roles at the same time, could have been the first evolvable entity on the evolutionary path to the first living cell. We have developed the Metabolically Coupled Replicator System (MCRS), a spatially explicit simulation modelling approach to prebiotic RNA-World evolution on mineral surfaces, in which we incorporate the most important experimental facts and theoretical considerations to comply with recent knowledge on RNA and prebiotic evolution. In this paper the MCRS model framework has been extended in order to investigate the dynamical and evolutionary consequences of adding an important physico-chemical detail, namely explicit replicator structure - nucleotide sequence and 2D folding calculated from thermodynamical criteria - and their possible mutational changes, to the assumptions of a previously less detailed toy model. Results: For each mutable nucleotide sequence the corresponding 2D folded structure with minimum free energy is calculated, which in turn is used to determine the fitness components (degradation rate, replicability and metabolic enzyme activity) of the replicator. We show that the community of such replicators providing the monomer supply for their own replication by evolving metabolic enzyme activities features an improved propensity for stable coexistence and structural adaptation. These evolutionary advantages are due to the emergent uniformity of metabolic replicator fitnesses imposed on the community by local group selection and attained through replicator trait convergence, i.e., the tendency of replicator lengths, ribozyme activities and population sizes to become similar between the coevolving replicator species that are otherwise both structurally and functionally different. Conclusions: In the most general terms it is the surprisingly high extra viability of the metabolic replicator system that the present model adds to the MCRS concept of the origin of life. Surface-bound, metabolically coupled RNA replicators tend to evolve different, enzymatically active sites within thermodynamically stable secondary structures, and the system as a whole evolves towards the robust coexistence of a complete set of such ribozymes driving the metabolism producing monomers for their own replication. Reviewers: This article was reviewed by Gáspár Jékely, Anthony Poole and Armen Mulkidjanian © 2015 Könnyu et al.; licensee BioMed Central.

Szathmary E.,Parmenides Center for the Conceptual Foundations of Science | Szathmary E.,Eotvos Lorand University
Journal of Theoretical Biology | Year: 2015

With his chemoton theory theoretical biologist and chemical engineer Tibor Gánti was one of the most outstanding intellects behind systems chemistry and the at the foundations of theoretical biology. A brief review of his oeuvre is presented. This essay introduces a special issue dedicated to his memory. © 2015 Published by Elsevier Ltd.

Ferdinandy B.,Eotvos Lorand University | Mones E.,Eotvos Lorand University | Vicsek T.,Eotvos Lorand University | Muller V.,Eotvos Lorand University | Muller V.,Parmenides Center for the Conceptual Foundations of Science
PLoS Computational Biology | Year: 2015

Outside Africa, the global phylogeography of HIV is characterized by compartmentalized local epidemics that are typically dominated by a single subtype, which indicates strong founder effects. We hypothesized that the competition of viral strains at the epidemic level may involve an advantage of the resident strain that was the first to colonize a population. Such an effect would slow down the invasion of new strains, and thus also the diversification of the epidemic. We developed a stochastic modelling framework to simulate HIV epidemics over dynamic contact networks. We simulated epidemics in which the second strain was introduced into a population where the first strain had established a steady-state epidemic, and assessed whether, and on what time scale, the second strain was able to spread in the population. Simulations were parameterized based on empirical data; we tested scenarios with varying levels of overall prevalence. The spread of the second strain occurred on a much slower time scale compared with the initial expansion of the first strain. With strains of equal transmission efficiency, the second strain was unable to invade on a time scale relevant for the history of the HIV pandemic. To become dominant over a time scale of decades, the second strain needed considerable (>25%) advantage in transmission efficiency over the resident strain. The inhibition effect was weaker if the second strain was introduced while the first strain was still in its growth phase. We also tested how possible mechanisms of interference (inhibition of superinfection, depletion of highly connected hubs in the network, one-time acute peak of infectiousness) contribute to the inhibition effect. Our simulations confirmed a strong first comer advantage in the competition dynamics of HIV at the population level, which may explain the global phylogeography of the virus and may influence the future evolution of the pandemic. © 2015 Ferdinandy et al.

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