30 research outputs found

    Learning mitigates genetic drift.

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    Genetic drift is a basic evolutionary principle describing random changes in allelic frequencies, with far-reaching consequences in various topics ranging from species conservation efforts to speciation. The conventional approach assumes that genetic drift has the same effect on all populations undergoing the same changes in size, regardless of different non-reproductive behaviors and history of the populations. However, here we reason that processes leading to a systematic increase of individuals` chances of survival, such as learning or immunological memory, can mitigate loss of genetic diversity caused by genetic drift even if the overall mortality rate in the population does not change. We further test this notion in an agent-based model with overlapping generations, monitoring allele numbers in a population of prey, either able or not able to learn from successfully escaping predators' attacks. Importantly, both these populations start with the same effective size and have the same and constant overall mortality rates. Our results demonstrate that even under these conditions, learning can mitigate loss of genetic diversity caused by drift, by creating a pool of harder-to-die individuals that protect alleles they carry from extinction. Furthermore, this effect holds regardless if the population is haploid or diploid or whether it reproduces sexually or asexually. These findings may be of importance not only for basic evolutionary theory but also for other fields using the concept of genetic drift

    Does Sex-Selective Predation Stabilize or Destabilize Predator-Prey Dynamics?

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    Background: Little is known about the impact of prey sexual dimorphism on predator-prey dynamics and the impact of sexselective harvesting and trophy hunting on long-term stability of exploited populations. Methodology and Principal Findings: We review the quantitative evidence for sex-selective predation and study its longterm consequences using several simple predator-prey models. These models can be also interpreted in terms of feedback between harvesting effort and population size of the harvested species under open-access exploitation. Among the 81 predator-prey pairs found in the literature, male bias in predation is 2.3 times as common as female bias. We show that long-term effects of sex-selective predation depend on the interplay of predation bias and prey mating system. Predation on the ‘less limiting’ prey sex can yield a stable predator-prey equilibrium, while predation on the other sex usually destabilizes the dynamics and promotes population collapses. For prey mating systems that we consider, males are less limiting except for polyandry and polyandrogyny, and male-biased predation alone on such prey can stabilize otherwise unstable dynamics. On the contrary, our results suggest that female-biased predation on polygynous, polygynandrous or monogamous prey requires other stabilizing mechanisms to persist. Conclusions and Significance: Our modelling results suggest that the observed skew towards male-biased predation might reflect, in addition to sexual selection, the evolutionary history of predator-prey interactions. More focus on these phenomena can yield additional and interesting insights as to which mechanisms maintain the persistence of predator-prey pairs over ecological and evolutionary timescales. Our results can also have implications for long-term sustainability of harvesting and trophy hunting of sexually dimorphic species

    When Mathematics Meets Biology: Mathematical Epidemiology

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    summary:Středověká morová epidemie způsobila smrt asi 17-22 % světové populace, z toho asi 30-60 % evropské populace, a trvalo zhruba 200 let, než se světová populace vrátila na svou původní úroveň. Epidemie dnes často zmiňované španělské chřipky v letech 1918-1920 vedla ke smrti přibližně 3-5 % světové populace. Svědky méně závažných, avšak stále dramatických epidemií jsme i v současnosti. Pandemie těžkého akutního respiračního syndromu (SARS) mezi roky 2002 a 2004, pandemie prasečí chřipky způsobené kmenem H1N1 v letech 2009-2010, či nedávná epidemie eboly v západní Africe nám neustále připomínají, že boj proti infekcím přes úspěšné vymýcení pravých neštovic zdaleka nekončí. Naopak, objevují se nové nemoci, ale také rezistentní kmeny nemocí známých. Už dlouho je naším pomocníkem při snaze porozumět šíření infekcí a bojovat s nimi také matematika. Představíme si průkopníky matematické epidemiologie, ale také moderní aplikace matematických modelů dynamiky infekčních nemocí pro kontrolu škůdců či tvorbu plánů pro zvládání potenciálních chřipkových pandemií

    More intense symptoms, more treatment, more drug-resistance: coevolution of virulence and drug-resistance

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    A recommendation – based on reviews by Three anonymous reviewers – of the article: Alizon S (2020) Treating symptomatic infections and the co-evolution of virulence and drug resistance. bioRxiv, 2020.02.29.970905, ver. 3 peer-reviewed and recommended by PCI Evol Biol. https://doi.org/10.1101/2020.02.29.97090
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