RESUMO
The extinction rate of populations is predicted to rise under increasing rates of environmental change. If a population experiencing increasingly stressful conditions lacks appropriate phenotypic plasticity or access to more suitable habitats, then genetic change may be the only way to avoid extinction. Evolutionary rescue from extinction occurs when natural selection enriches a population for more stress-tolerant genetic variants. Some experimental studies have shown that lower rates of environmental change lead to more adapted populations or fewer extinctions. However, there has been little focus on the genetic changes that underlie evolutionary rescue. Here we demonstrate that some evolutionary trajectories are contingent on a lower rate of environmental change. We allowed hundreds of populations of Escherichia coli to evolve under variable rates of increase in concentration of the antibiotic rifampicin. We then genetically engineered all combinations of mutations from isolates evolved under lower rates of environmental change. By assessing fitness of these engineered strains across a range of drug concentrations, we show that certain genotypes are evolutionarily inaccessible under rapid environmental change. Rapidly deteriorating environments not only limit mutational opportunities by lowering population size, but they can also eliminate sets of mutations as evolutionary options. As anthropogenic activities are leading to environmental change at unprecedented rapidity, it is critical to understand how the rate of environmental change affects both demographic and genetic underpinnings of evolutionary rescue.
Assuntos
Adaptação Fisiológica/genética , Evolução Biológica , Mudança Climática , Extinção Biológica , Aptidão Genética/genética , Modelos Biológicos , Mutagênese/genética , Adaptação Fisiológica/efeitos dos fármacos , Antibióticos Antituberculose/farmacologia , Mudança Climática/mortalidade , Mudança Climática/estatística & dados numéricos , Contagem de Colônia Microbiana , Análise Mutacional de DNA , RNA Polimerases Dirigidas por DNA , Relação Dose-Resposta a Droga , Escherichia coli/citologia , Escherichia coli/efeitos dos fármacos , Escherichia coli/genética , Escherichia coli/isolamento & purificação , Proteínas de Escherichia coli/genética , Genes Bacterianos/genética , Aptidão Genética/efeitos dos fármacos , Genótipo , Atividades Humanas , Testes de Sensibilidade Microbiana , Mutagênese/efeitos dos fármacos , Mutação/genética , Densidade Demográfica , Rifampina/farmacologia , Fatores de TempoRESUMO
Understanding pathogen infectivity and virulence requires combining insights from epidemiology, ecology, evolution and genetics. Although theoretical work in these fields has identified population structure as important for pathogen life-history evolution, experimental tests are scarce. Here, we explore the impact of population structure on life-history evolution in phage T4, a viral pathogen of Escherichia coli. The host-pathogen system is propagated as a metapopulation in which migration between subpopulations is either spatially restricted or unrestricted. Restricted migration favours pathogens with low infectivity and low virulence. Unrestricted migration favours pathogens that enter and exit their hosts quickly, although they are less productive owing to rapid extirpation of the host population. The rise of such 'rapacious' phage produces a 'tragedy of the commons', in which better competitors lower productivity. We have now identified a genetic basis for a rapacious life history. Mutations at a single locus (rI) cause increased virulence and are sufficient to account for a negative relationship between phage competitive ability and productivity. A higher frequency of rI mutants under unrestricted migration signifies the evolution of rapaciousness in this treatment. Conversely, spatially restricted migration favours a more 'prudent' pathogen strategy, in which the tragedy of the commons is averted. As our results illustrate, profound epidemiological and ecological consequences of life-history evolution in a pathogen can have a simple genetic cause.