The impact of population size on the evolution of asexual microbes on smooth versus rugged fitness landscapes

<p>Abstract</p> <p>Background</p> <p>It is commonly thought that large asexual populations evolve more rapidly than smaller ones, due to their increased rate of beneficial mutations. Less clear is how population size influences the level of fitness an asexual population can attain. Here, we simulate the evolution of bacteria in repeated serial passage experiments to explore how features such as fitness landscape ruggedness, the size of the mutational target under selection, and the mutation supply rate, interact to affect the evolution of microbial populations of different sizes.</p> <p>Results</p> <p>We find that if the fitness landscape has many local peaks, there can be a trade-off between the rate of adaptation and the potential to reach high fitness peaks. This result derives from the fact that whereas large populations evolve mostly deterministically and often become trapped on local fitness peaks, smaller populations can follow more stochastic evolutionary paths and thus locate higher fitness peaks. We also find that the target size of adaptation and the mutation rate interact with population size to influence the trade-off between rate of adaptation and final fitness.</p> <p>Conclusion</p> <p>Our study suggests that the optimal population size for adaptation depends on the details of the environment and on the importance of either the ability to evolve rapidly or to reach high fitness levels.</p

Oscillations in continuous culture populations of Streptococcus pneumoniae: population dynamics and the evolution of clonal suicide

Agents that kill or induce suicide in the organisms that produce them or other individuals of the same genotype are intriguing puzzles for ecologists and evolutionary biologists. When those organisms are pathogenic bacteria, these suicidal toxins have the added appeal as candidates for the development of narrow spectrum antibiotics to kill the pathogens that produce them. We show that when clinical as well as laboratory strains of Streptococcus pneumoniae are maintained in continuous culture (chemostats), their densities oscillate by as much as five orders of magnitude with an apparently constant period. This dynamic, which is unanticipated for single clones of bacteria in chemostats, can be attributed to population-wide die-offs and recoveries. Using a combination of mathematical models and experiments with S. pneumoniae, we present evidence that these die-offs can be attributed to the autocatalytic production of a toxin that lyses or induces autolysis in members of the clone that produces it. This toxin, which our evidence indicates is a protein, appears to be novel; S. pneumoniae genetic constructs knocked out for lytA and other genes coding for known candidates for this agent oscillate in chemostat culture. Since this toxin lyses different strains of S. pneumoniae as well as other closely related species of Streptococcus, we propose that its ecological role is as an allelopathic agent. Using a mathematical model, we explore the conditions under which toxins that kill members of the same clone that produces them can prevent established populations from invasion by different strains of the same or other species. We postulate that the production of the toxin observed here as well as other bacteria-produced toxins that kill members of the same genotype, ‘clonal suicide’, evolved and are maintained to prevent colonization of established populations by different strains of the same and closely related species

Pherotype polymorphism in Streptococcus pneumoniae has no obvious effects on population structure and recombination

Natural transformation in the Gram-positive pathogen Streptococcus pneumoniae occurs when cells become “competent”, a state that is induced in response to high extracellular concentrations of a secreted peptide signal called CSP (Competence Stimulating Peptide) encoded by the comC locus. Two main CSP signal types (pherotypes) are known to dominate the pherotype diversity across strains. Using 4,089 fully sequenced pneumococcal genomes, we confirm that pneumococcal populations are highly genetically structured and that there is significant variation among diverged populations in pherotype frequencies; most carry only a single pherotype. Moreover, we find that the relative frequencies of the two dominant pherotypes significantly vary within a small range across geographical sites. It has been variously proposed that pherotypes either promote genetic exchange among cells expressing the same pherotype, or conversely that they promote recombination between strains bearing different pherotypes. We attempt to distinguish these hypotheses using a bioinformatics approach by estimating recombination frequencies within and between pherotypes across 4,089 full genomes. Despite underlying population structure, we observe extensive recombination between populations; additionally, we found significantly higher (although marginal) rates of genetic exchange between strains expressing different pherotypes than among isolates carrying the same pherotype. Our results indicate that pherotypes do not restrict, and may even slightly facilitate, recombination between strains; however, these marginal effects suggest the more likely possibility that the cause of CSP polymorphism lies outside of its effects on transformation. Our results suggest that the CSP balanced polymorphism does not causally underlie population differentiation. Therefore, when strains carrying different pherotypes encounter one another during co-colonization, genetic exchange can occur without restriction

Pherotype Polymorphism in Streptococcus pneumoniae Has No Obvious Effects on Population Structure and Recombination.

Natural transformation in the Gram-positive pathogen Streptococcus pneumoniae occurs when cells become "competent," a state that is induced in response to high extracellular concentrations of a secreted peptide signal called competence stimulating peptide (CSP) encoded by the comC locus. Two main CSP signal types (pherotypes) are known to dominate the pherotype diversity across strains. Using 4,089 fully sequenced pneumococcal genomes, we confirm that pneumococcal populations are highly genetically structured and that there is significant variation among diverged populations in pherotype frequencies; most carry only a single pherotype. Moreover, we find that the relative frequencies of the two dominant pherotypes significantly vary within a small range across geographical sites. It has been variously proposed that pherotypes either promote genetic exchange among cells expressing the same pherotype, or conversely that they promote recombination between strains bearing different pherotypes. We attempt to distinguish these hypotheses using a bioinformatics approach by estimating recombination frequencies within and between pherotypes across 4,089 full genomes. Despite underlying population structure, we observe extensive recombination between populations; additionally, we found significantly higher (although marginal) rates of genetic exchange between strains expressing different pherotypes than among isolates carrying the same pherotype. Our results indicate that pherotypes do not restrict, and may even slightly facilitate, recombination between strains; however, these marginal effects suggest the more likely possibility that the cause of CSP polymorphism lies outside of its effects on transformation. Our results suggest that the CSP balanced polymorphism does not causally underlie population differentiation. Therefore, when strains carrying different pherotypes encounter one another during cocolonization, genetic exchange can occur without restriction

Effect of carcass contamination on necrophagous invertebrate performance

Background The breakdown of dead organic matter is driven by a diverse array of organisms and is an important process increasingly impacted by a range of contaminants. While many studies have documented how contaminants affect food webs that are fueled by decaying plant litters, much less is known about how contaminants affect organisms that rely on dead animal material. Here, we begin to explore the effects of food contamination—using silver nanoparticles (AgNPs) as a model contaminant—on the carrion beetle Nicrophorus vespilloides that buries carcasses of small vertebrates in soils as food source and larval nursing grounds. Results Our data show that a single ingestion of a non-lethal dose of 1 μg mL−1 AgNPs by adult female beetles does not affect overall gut microbial activity but results in shifts in the gut microbial community composition towards pathogens including Alcaligenes, Morganella, and Pseudomonas. While no effects were observed in offspring clutch size, some reductions were visible in clutch weight, number of larvae, and number of eclosing pupae in exposed N. vespilloides in comparison with controls. Repeated ingestion of AgNPs over several weeks led to a decrease in survival of adult beetles, suggesting that more environmentally realistic exposure scenarios can directly affect the success of carcass-feeding animals. Conclusions Sub-lethal carcass contamination with a model pollutant can affect the gut microbial composition in female beetles and reduce offspring fitness. This encourages consideration of currently overlooked propagation routes of contaminants through necrophagous food webs and inherent consequences for ecological and evolutionary processes.publishedVersio

Killing as means of promoting biodiversity

Abstract Bacteriocins are usually viewed as the effective weapons of bacterial killers. However, killing competitors with bacteriocins may be not only a means of eliminating other strains, but also a crucial unappreciated mechanism promoting bacterial diversity. In the present short review, we summarize recent empirical and theoretical studies examining the role bacteriocins that may play in driving and maintaining diversity among microbes. We conclude by highlighting limitations of current models and suggest directions for future studies

Expression of Streptococcus pneumoniae Bacteriocins Is Induced by Antibiotics via Regulatory Interplay with the Competence System

Pneumococcal bacteriocins (pneumocins) are antibacterial toxins that mediate intra-species competition within the human host. However, the triggers of pneumocin expression are poorly understood. Using RNA-sequencing, we mapped the regulon of the pneumocin cluster (blp) of Streptococcus pneumoniae D39. Furthermore, by analogy with pneumococcal competence, we show that several antibiotics activate the blp-genes. Using real-time gene expression measurements we show that while the promoter driving expression of the two-component regulatory system blpR/H is constitutive, the remaining blp-promoters that control pneumocin expression, immunity and the inducer peptide BlpC, are pH-dependent and induced in the late exponential phase. Intriguingly, competence for genetic transformation, mediated by the paralogous ComD/E two-component quorum system, is induced by the same environmental cues. To test for interplay between these regulatory systems, we quantified the regulatory response to the addition of synthetic BlpC and competence-stimulating peptide (CSP). Supporting the idea of such interplay, we found that immediately upon addition of CSP, the blp-promoters were activated in a comD/E-dependent manner. After a delay, blp-expression was highly induced and was strictly dependent on blpRH and blpC. This raised the question of the mechanism of BlpC export, since bioinformatic analysis showed that the genes encoding the putative exporter for BlpC, blpAB, are not intact in strain D39 and most other strains. By contrast, all sequenced pneumococcal strains contain intact comAB genes, encoding the transport system for CSP. Consistent with the idea that comAB mediate BlpC export, we finally show that high-level expression of the blp-genes requires comAB. Together, our results demonstrate that regulation of pneumocin expression is intertwined with competence, explaining why certain antibiotics induce blp-expression. Antibiotic-induced pneumocin expression might therefore have unpredictable consequences on pneumococcal colonization dynamics by activating genes that mediate intra-specific interference competition