1,721,006 research outputs found
Encounters with archaic hominins
No full textThe presence of Neanderthal DNA fragments in the genomes of modern humans from Europe and East Asia indicates multiple episodes of interbreeding between Neanderthals and the ancestors of both populations. © 2018, Springer Nature Limited
The complexity of understanding others as the evolutionary origin of empathy and emotional contagion
Full text linkContagious yawning, emotional contagion and empathy are characterized by the activation of similar neurophysiological states or responses in an observed individual and an observer. For example, it is hard to keep one’s mouth closed when imagining someone yawning, or not feeling distressed while observing other individuals perceiving pain. The evolutionary origin of these widespread phenomena is unclear, since a direct benefit is not always apparent. We explore a game theoretical model for the evolution of mind-reading strategies, used to predict and respond to others’ behavior. In particular we explore the evolutionary scenarios favoring simulative strategies, which recruit overlapping neural circuits when performing as well as when observing a specific behavior. We show that these mechanisms are advantageous in complex environments, by allowing an observer to use information about its own behavior to interpret that of others. However, without inhibition of the recruited neural circuits, the observer would perform the corresponding downstream action, rather than produce the appropriate social response. We identify evolutionary trade-offs that could hinder this inhibition, leading to emotional contagion as a by-product of mind-reading. The interaction of this model with kinship is complex. We show that empathy likely evolved in a scenario where kin- and other indirect benefits co-opt strategies originally evolved for mind-reading, and that this model explains observed patterns of emotional contagion with kin or group members. © 2019, The Author(s)
Selective strolls: Fixation and extinction in diploids are slower for weakly selected mutations than for neutral ones
No full textIn finite populations, an allele disappears or reaches fixation due to two main forces, selection and drift. Selection is generally thought to accelerate the process: a selected mutation will reach fixation faster than a neutral one, and a disadvantageous one will quickly disappear from the population. We show that even in simple diploid populations, this is often not true. Dominance and recessivity unexpectedly slow down the evolutionary process for weakly selected alleles. In particular, slightly advantageous dominant and mildly deleterious recessive mutations reach fixation slightly more slowly than neutral ones (at most 5%). This phenomenon determines genetic signatures opposite to those expected under strong selection, such as increased instead of decreased genetic diversity around the selected site. Furthermore, we characterize a new phenomenon: mildly deleterious recessive alleles, thought to represent a wide fraction of newly arising mutations, on average survive in a population slightly longer than neutral ones, before getting lost. Consequently, these mutations are on average slightly older than neutral ones, in contrast with previous expectations. Furthermore, they slightly increase the amount of weakly deleterious polymorphisms, as a consequence of the longer unconditional sojourn times compared to neutral mutations. © 2015 by the Genetics Society of America
Cognitive Twists: The Coevolution of Learning and Genes in Human Cognition
No full textIn this paper, we propose the expression cognitive twists for cognitive mechanisms that result from the coevolution of genes and learning. Evidence is available that at least some cultural learning mechanisms, such as imitation and language, have evolved genetically under the pressure produced by culture, even though they are mostly acquired through domain-general learning during development. Although the existence of these mechanisms is consistent with evolutionary theory, their importance has not been sufficiently emphasized by mind-centered accounts of human cognitive evolution, namely evolutionary psychology and cultural evolutionary psychology. We provide concrete examples of cognitive twists, such as vocal imitation. Genetic changes in action-perception matching circuits suggest that human imitation and perhaps language are cognitive twists, namely plastic, learnable, yet genetically evolved cognitive mechanisms. We conclude that cognitive twists depict plausible evolutionary scenarios for the evolution of cognition in Homo sapiens
Cognitive Twists: The Coevolution of Learning and Genes in Human Cognition
No full textIn this paper, we propose the expression cognitive twists for cognitive mechanisms that result from the coevolution of genes and learning. Evidence is available that at least some cultural learning mechanisms, such as imitation and language, have evolved genetically under the pressure produced by culture, even though they are mostly acquired through domain-general learning during development. Although the existence of these mechanisms is consistent with evolutionary theory, their importance has not been sufficiently emphasized by mind-centered accounts of human cognitive evolution, namely evolutionary psychology and cultural evolutionary psychology. We provide concrete examples of cognitive twists, such as vocal imitation. Genetic changes in action-perception matching circuits suggest that human imitation and perhaps language are cognitive twists, namely plastic, learnable, yet genetically evolved cognitive mechanisms. We conclude that cognitive twists depict plausible evolutionary scenarios for the evolution of cognition in Homo sapiens
Better support for a small effective population size of Neandertals and a long shared history of Neandertals and Denisovans
No full textNational Academy of Science
On the fitness of informative cues in complex environments
No full textTo be able to deal with uncertainty is of primary importance to all organisms. When cues provide information about the state of the environment, organisms can use them to respond flexibly. Thus information can provide fitness advantages. Without environmental cues, an organism can reduce the risks of environmental uncertainty by hedging its bets across different scenarios. Risk mitigation is then possible by adopting a life-history of bet-hedging, either randomly switching between phenotypes (diversifying bet-hedging) or adopting intermediate phenotypes (conservative bet-hedging). Hence, understanding patterns of bet-hedging is necessary in order to quantify the fitness benefit of environmental cues, since it provides a baseline fitness in the absence of informative cues. Quantifying fitness benefits in terms of mutual information reveals deep connections between Darwinian evolution and information theory. However, physiological constraints or complex ecological scenarios often lead to the number of environmental states to exceed that of potential phenotypes, or a single intermediate phenotype is adopted, as in the case of conservative bet-hedging. Incorporating these biological complexities, we generalise the relationship between information theory and Darwinian fitness. Sophisticated bet-hedging strategies combining diversifying and conservative bet-hedging - can then evolve. We show that, counterintuitively, environmental complexity can reduce, rather than increase, the number of phenotypes that an organism can adopt. In conclusion, we develop an information-theoretic extensible approach for investigating and quantifying fitness in ecological studies
Population Dynamics and Structural Effects at Short and Long Range Support the Hypothesis of the Selective Advantage of the G614 SARS-CoV-2 Spike Variant
Full text linkSARS-CoV-2 epidemics quickly propagated worldwide, sorting virus genomic variants in newly established propagules of infections. Stochasticity in transmission within and between countries or an actual selective advantage could explain the global high frequency reached by some genomic variants. Using statistical analyses, demographic reconstructions, and molecular dynamics simulations, we show that the globally invasive G614 spike variant 1) underwent a significant demographic expansion in most countries explained neither by stochastic effects nor by overrepresentation in clinical samples, 2) increases the spike S1/S2 furin-like site conformational plasticity (short-range effect), and 3) modifies the internal motion of the receptor-binding domain affecting its cross-connection with other functional domains (long-range effect). Our results support the hypothesis of a selective advantage at the basis of the spread of the G614 variant, which we suggest may be due to structural modification of the spike protein at the S1/S2 proteolytic site, and provide structural information to guide the design of variant-specific drugs
Turning vice into virtue: Using batch-effects to detect errors in large genomic data sets
No full textIt is often unavoidable to combine data fromdifferent sequencing centers or sequencing platformswhen compiling data sets with a large number of individuals.However, the different data are likely to contain specific systematic errors that will appear as SNPs.Here,wedevise amethod to detect systematic errors in combined data sets. Tomeasure quality differences between individual genomes, we study pairs of variants that reside on different chromosomes and co-occur in individuals. The abundance of these pairs of variants in different genomes is then used to detect systematic errors due to batch effects. Applying ourmethod to the 1000 Genomes data set,we find that coding regions are enriched for errors,where 1%of the higher frequency variants are predicted to be erroneous, whereas errors outside of coding regions are much rarer (<0.001%). As expected, predicted errors are found less often than other variants in a data set that was generated with a different sequencing technology, indicating that many of the candidates are indeed errors. However, predicted 1000 Genomes errors are also found in other large data sets; our observation is thus not specific to the 1000Genomes data set.Our results show that batch effects can be turned into a virtue by using the resulting variation in large scale data sets to detect systematic errors. © 2018 Oxford University Press. All rights reserved
The heat-inducible transcription factor HsfA2 enhances anoxia tolerance in Arabidopsis
Full text linkAnoxia induces several heat shock proteins, and a mild heat pretreatment can acclimatize Arabidopsis (Arabidopsis thaliana) seedlings to subsequent anoxic treatment. In this study, we analyzed the response of Arabidopsis seedlings to anoxia, heat, and combined heat + anoxia stress. A significant overlap between the anoxic and the heat responses was observed by whole-genome microarray analysis. Among the transcription factors induced by both heat and anoxia, the heat shock factor A2 (HsfA2), known to be involved in Arabidopsis acclimation to heat and to other abiotic stresses, was strongly induced by anoxia. Heat-dependent acclimation to anoxia is lost in an HsfA2 knockout mutant (hsfa2) as well as in a double mutant for the constitutively expressed HsfA1a/HsfA1b (hsfA1a/1b), indicating that these three heat shock factors cooperate to confer anoxia tolerance. Arabidopsis seedlings that overexpress HsfA2 showed an increased expression of several known targets of this transcription factor and were markedly more tolerant to anoxia as well as to submergence. Anoxia failed to induce HsfA2 target proteins in wild-type seedlings, while overexpression of HsfA2 resulted in the production of HsfA2 targets under anoxia, correlating well with the low anoxia tolerance experiments. These results indicate that there is a considerable overlap between the molecular mechanisms of heat and anoxia tolerance and that HsfA2 is a player in these mechanisms. © 2010 American Society of Plant Biologists
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