Evolution of commensal bacteria in the intestinal tract of mice

Sousa, Ana; Frazão, Nelson; Ramiro, Ricardo S.; Gordo, Isabel

doi:10.1016/j.mib.2017.05.007

Cited by 34 publications

(33 citation statements)

References 66 publications

(85 reference statements)

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“…While acquisition of new DNA requires specific ecological contexts (i.e. : the presence of donor bacteria), adaptive mutations (potentially including resistance mutations) are continuously generated at rates that can be as high as ~10 -5 per cell per generation [11][12][13]. Furthermore, mutations leading to genomic rearrangements (insertions, deletions, duplications, inversions) occur at an even higher rate (10 -3 -10 -5 per cell per generation) which can accelerate the rate of acquiring AR [14,15].…”

Section: Emergence Of Bacterial Antibiotic Resistancementioning

confidence: 99%

Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance

Durão

Balbontín

Gordo

2018

Trends in Microbiology

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Antibiotics target essential cellular functions but bacteria can become resistant by acquiring either exogenous resistance genes or chromosomal mutations. Resistance mutations typically occur in genes encoding essential functions; these mutations are therefore generally detrimental in the absence of drugs. However, bacteria can reduce this handicap by acquiring additional mutations, known as compensatory mutations. Genetic interactions (epistasis) either with the background or between resistances (in multiresistant bacteria) dramatically affect the fitness cost of antibiotic resistance and its compensation, therefore shaping dissemination of antibiotic resistance mutations. This Review summarizes current knowledge on the evolutionary mechanisms influencing maintenance of resistance mediated by chromosomal mutations, focusing on their fitness cost, compensatory evolution, epistasis, and the effect of the environment on these processes.

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Section: Emergence Of Bacterial Antibiotic Resistancementioning

confidence: 99%

Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance

Durão

Balbontín

Gordo

2018

Trends in Microbiology

Self Cite

197

131

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“…Importantly, strain level variation is key for multiple phenotypes ranging from antibiotic resistance and virulence to colonisation resistance (e.g., [9][10][11]). However, little is known about how different evolutionary mechanisms-such as mutation, recombination, migration, genetic drift, and natural selection-shape bacterial genetic diversity within the mammalian gut [12].…”

Section: Introductionmentioning

confidence: 99%

Low mutational load and high mutation rate variation in gut commensal bacteria

et al. 2020

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Bacteria generally live in species-rich communities, such as the gut microbiota. Yet little is known about bacterial evolution in natural ecosystems. Here, we followed the longterm evolution of commensal Escherichia coli in the mouse gut. We observe the emergence of mutation rate polymorphism, ranging from wild-type levels to 1,000-fold higher. By combining experiments, whole-genome sequencing, and in silico simulations, we identify the molecular causes and explore the evolutionary conditions allowing these hypermutators to emerge and coexist within the microbiota. The hypermutator phenotype is caused by mutations in DNA polymerase III proofreading and catalytic subunits, which increase mutation rate by approximately 1,000-fold and stabilise hypermutator fitness, respectively. Strong mutation rate variation persists for >1,000 generations, with coexistence between lineages carrying 4 to >600 mutations. The in vivo molecular evolution pattern is consistent with fitness effects of deleterious mutations s d � 10 −4 /generation, assuming a constant effect or exponentially distributed effects with a constant mean. Such effects are lower than typical in vitro estimates, leading to a low mutational load, an inference that is observed in in vivo and in vitro competitions. Despite large numbers of deleterious mutations, we identify multiple beneficial mutations that do not reach fixation over long periods of time. This indicates that the dynamics of beneficial mutations are not shaped by constant positive Darwinian selection but could be explained by other evolutionary mechanisms that maintain genetic diversity. Thus, microbial evolution in the gut is likely characterised by partial sweeps of beneficial mutations combined with hitchhiking of slightly deleterious mutations, which take a long time to be purged because they impose a low mutational load. The combination of these two processes could allow for the longterm maintenance of intraspecies genetic diversity, including mutation rate polymorphism. These results are consistent with the pattern of genetic polymorphism that is emerging from metagenomics studies of the human gut microbiota, suggesting that we have identified key evolutionary processes shaping the genetic composition of this community.

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“…The assembly of this community is initiated during the neonate stage and it suffers markedly changes in composition during the first years of life [1]. The population dynamics of this community are thought to be determined by ecoevolutionary processes [2][3][4]. While our understanding of the gut microbiota is still far from complete, it is now evident that it has a crucial impact on health, affecting a plethora of host functions that include immunity, development and nutrition [5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Specific Eco-evolutionary Contexts in the Mouse Gut Reveal Escherichia coli Metabolic Versatility

et al. 2020

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Members of the gut microbiota are thought to experience strong competition for nutrients. However, how such competition shapes their evolutionary dynamics and depends on intraand interspecies interactions is poorly known. Here we tested the hypothesis that Escherichia coli evolution in the mouse gut is more predictable across hosts in absence of interspecies competition than in the presence of other microbial species. Supporting this hypothesis, we observed a specific genetic adaptation in lrp, a gene encoding a global regulator of amino acid metabolism, predictably selected in germ-free mice two weeks after mono-colonization. Analysis of gut metabolites established that the lpr mutations increase E. coli ability to compete for amino acids and identified serine and threonine as the metabolites preferentially consumed by E. coli in the mono-colonized mouse gut. Preference for serine consumption was further demonstrated by testing a set of mutants in vitro and in vivo that showed loss of advantage of a lrp mutant impaired in serine metabolism. Remarkably, the presence of a single additional member of the microbiota (Blautia coccoides) was enough to alter the gut metabolic profile and consequently the evolutionary path of E. coli. In this environment, the lrp mutations did not conferred advantage to E. coli and genes involved in anaerobic respiration were selected instead, recapitulating the ecoevolutionary context from mice with a complex microbiota. Together, these results highlight the metabolic plasticity of E. coli and its extreme evolutionary versatility, tailored to the specific ecology it experiences in the gut.

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Evolution of commensal bacteria in the intestinal tract of mice

Cited by 34 publications

References 66 publications

Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance

Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance

Low mutational load and high mutation rate variation in gut commensal bacteria

Specific Eco-evolutionary Contexts in the Mouse Gut Reveal Escherichia coli Metabolic Versatility

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