Publications by year
In Press
Pons BJ, Dimitriu T, Westra ER, van Houte S (In Press). Antibiotics that affect translation can antagonize phage infectivity by interfering with the deployment of counter-defences.
Abstract:
Antibiotics that affect translation can antagonize phage infectivity by interfering with the deployment of counter-defences
AbstractIt is becoming increasingly clear that antibiotics can both positively and negatively impact the infectivity of bacteriophages (phage), but the underlying mechanisms often remain unclear. Here we demonstrate that antibiotics that target the protein translation machinery can fundamentally alter the outcome of bacteria-phage interactions by interfering with the production of phage-encoded counter-defence proteins. Specifically, using Pseudomonas aeruginosa PA14 and phage DMS3vir as a model, we show that bacteria with CRISPR-Cas immune systems have elevated levels of immunity against phage that encode anti-CRISPR (acr) genes when translation inhibitors are present in the environment. CRISPR-Cas are highly prevalent defence systems that enable bacteria to detect and destroy phage genomes in a sequence-specific manner. In response, many phages encode acr genes that are expressed immediately following infection to inhibit key steps of the CRISPR-Cas immune response. Our data show that while phage carrying acr genes can amplify efficiently on bacteria with CRISPR-Cas immune systems in the absence of antibiotics, the presence of antibiotics that act on protein translation prevents phage amplification, while protecting bacteria from lysis. These results help to understand how antibiotics-phage synergy and antagonism depend on the molecular interactions that define phage infectivity and host immunity.
Abstract.
Dimitriu T, Kurilovich E, Lapinska U, Severinov K, Pagliara S, Szczelkun MD, Westra ER (In Press). Bacteriostatic antibiotics promote the evolution of CRISPR-Cas immunity.
Abstract:
Bacteriostatic antibiotics promote the evolution of CRISPR-Cas immunity
AbstractPhage therapy can be used in combination with antibiotics to combat infections with bacterial pathogens1–3. However, bacteria can rapidly evolve phage resistance via receptor mutation, or using their CRISPR-Cas adaptive immune systems4, which insert short phage-derived sequences into CRISPR loci in the bacterial genome5 to guide sequence-specific cleavage of cognate sequences6. Unlike CRISPR-Cas immunity, mutation of the phage receptor leads to attenuated virulence when the opportunistic pathogen Pseudomonas aeruginosa is infected with its phage DMS3vir7, which underscores the need to predict how phage resistance evolves under clinically relevant conditions. Here, using eight antibiotics with various modes of action, we show that bacteriostatic antibiotics (which inhibit cell growth without killing) specifically promote evolution of CRISPR-Cas immunity in P. aeruginosa by slowing down phage development and providing more time for cells to acquire phage-derived sequences and mount an immune response. Our data show that some antimicrobial treatments can contribute to the evolution of phage-resistant pathogens with high virulence.
Abstract.
Pursey E, Dimitriu T, Paganelli FL, Westra ER, van Houte S (In Press). CRISPR-Cas is associated with fewer antibiotic resistance genes in bacterial pathogens.
Abstract:
CRISPR-Cas is associated with fewer antibiotic resistance genes in bacterial pathogens
AbstractThe acquisition of antibiotic resistance genes via horizontal gene transfer is a key driver of the rise in multidrug resistance amongst bacterial pathogens. Bacterial defence systems per definition restrict the influx of foreign genetic material, and may therefore limit the acquisition of antibiotic resistance. CRISPR-Cas adaptive immune systems are one of the most prevalent defences in bacteria, found in roughly half of bacterial genomes, but it has remained unclear if and how much they contribute to restricting the spread of antibiotic resistance. We analysed ~40,000 whole genomes comprising the full RefSeq dataset for 11 species of clinically important genera of human pathogens including Enterococcus, Staphylococcus, Acinetobacter and Pseudomonas. We modelled the association between CRISPR-Cas and indicators of horizontal gene transfer, and found that pathogens with a CRISPR-Cas system were less likely to carry antibiotic resistance genes than those lacking this defence system. Analysis of the mobile genetic elements targeted by CRISPR-Cas supports a model where this host defence system blocks important vectors of antibiotic resistance. These results suggest a potential “immunocompromised” state for multidrug-resistant strains that may be exploited in tailored interventions that rely on mobile genetic elements, such as phage or phagemids, to treat infections caused by bacterial pathogens.
Abstract.
Dimitriu T, Matthews A, Buckling A (In Press). Increased copy number couples the evolution of plasmid horizontal transmission and antibiotic resistance.
Abstract:
Increased copy number couples the evolution of plasmid horizontal transmission and antibiotic resistance
AbstractAntimicrobial resistance (AMR) in bacteria is commonly encoded on conjugative plasmids, mobile elements which can spread horizontally between hosts. Conjugative transfer disseminates AMR in communities but it remains unclear when and how high transfer rates evolve, and with which consequences. Here we studied experimentally the evolution of two antibiotic resistance encoding plasmids when confronted to different immigration rates of susceptible, plasmid-free hosts. While plasmid RP4 did not evolve detectably, plasmid R1 rapidly evolved up to 1000-fold increased transfer rates in the presence of susceptible hosts, at a cost to its host. Unexpectedly, most evolved plasmids also conferred to their hosts the ability to grow at high concentrations of antibiotics. The most common mutations in evolved plasmids were contained within thecopAgene which controls plasmid replication and copy number. EvolvedcopAvariants had elevated copy number, leading to both higher transfer rates and AMR. Due to these pleiotropic effects, host availability and antibiotics were each sufficient to select for highly transmissible plasmids conferring high levels of antibiotic resistance.
Abstract.
Dimitriu T, Andrew C. M, Buckling A (In Press). Increased copy number couples the evolution of plasmid horizontal transmission and plasmid-encoded antibiotic resistance.
Proceedings of the National Academy of Sciences of USAAbstract:
Increased copy number couples the evolution of plasmid horizontal transmission and plasmid-encoded antibiotic resistance.
Conjugative plasmids are mobile elements which spread horizontally between bacterial hosts, and often confer adaptive phenotypes, including antimicrobial resistance (AMR). Theory suggests that opportunities for horizontal transmission favour plasmids with higher transfer rates, whereas selection for plasmid carriage favour less mobile plasmids. However, little is known about the mechanisms leading to variation in transmission rates in natural plasmids or the resultant effects on their bacterial host. We investigated the evolution of AMR plasmids confronted with different immigration rates of susceptible hosts. Plasmid RP4 did not evolve in response to the manipulations, but plasmid R1 rapidly evolved up to 1000-fold increased transfer rates in the presence of susceptible hosts. Most evolved plasmids also conferred on their hosts the ability to grow at high concentrations of antibiotics. This was because plasmids evolved greater copy numbers, as a function of mutations in the copA gene controlling plasmid replication, causing both higher transfer rates and AMR. Reciprocally, plasmids with increased conjugation rates also evolved when selecting for high levels of AMR, despite the absence of susceptible hosts. Such correlated selection between plasmid transfer and AMR could increase the spread of AMR within populations and communities.
Abstract.
Pursey E, Dimitriu T, Gaze WH, Westra ER, van Houte S (In Press). Modelling the distribution of antimicrobial resistance genes across geography, climate, host species and phylogroup in 16,000 <i>E. coli</i> genomes.
Abstract:
Modelling the distribution of antimicrobial resistance genes across geography, climate, host species and phylogroup in 16,000 E. coli genomes
SummaryBackgroundE. coli is a highly diverse species that generates a huge global burden of antimicrobial-resistant infections. Although it is one of the most well-studied model organisms, we lack a synthesis of the genomic distribution of antimicrobial resistance (AMR) genes according to phylogenetic and ecological variables.MethodsWe implemented Mash-based phylogrouping on ∼16,000 RefSeq E. coli genomes, and statistically modelled the link between phylogroups, host species categories, geographic subregions, climate, and AMR genes. We predict the burden of AMR across these categories using several metrics including overall counts of resistance genes, multidrug- and extensively-drug resistant (MDR and XDR) classifications, and frequencies of extended-spectrum β-lactamase and carbapenemase genes.FindingsAMR burden was highly variable across all measures between phylogroups, host species, geographic locations and climates. Phylogroups spanning the commensal-pathogen spectrum were found with high levels of AMR. MDR genomes were highly prevalent in North Africa and South-Eastern Asia, while XDR isolates were more common in Eastern Asia. Wild birds were associated with the highest levels of XDR and carbapenemase-encoding isolates. Carbapenemases, MDR genomes and most blaCTX-M groups were positively associated with temperature.InterpretationThis study synthesises data on clinical, ecological and anthropogenic variables impacting AMR in E. coli on an unprecedented scale, modelling its burden across clinically-relevant measures. It highlights key findings with direct relevance to managing the global spread of AMR and understanding its ecology. Finally, it emphasizes knowledge gaps in public databases that, if investigated, would further develop our understanding of AMR in this important pathogen and the risk posed across contexts.FundingEU Horizon 2020 ProgrammeBiotechnology and Biological Sciences Research Council (BBSRC)
Abstract.
Dimitriu T, Marchant L, Buckling A, Raymond B (In Press). Plasmid transfer is biased towards close kin in bacteria from natural populations.
Abstract:
Plasmid transfer is biased towards close kin in bacteria from natural populations
AbstractPlasmids play a key role in microbial ecology and evolution, yet the determinants of plasmid transfer rates are poorly understood. Here we investigate the importance of genetic similarity between naturally co-occurringEscherichia coliisolates in the transfer of two plasmids (narrow-host-range R1 and broad-host-range RP4). We uncovered extensive variability, spanning over five orders of magnitude, in the ability of isolates to donate and receive plasmids. Overall, transfer was strongly biased towards clone-mates, but not correlated to genetic distance between donors and recipients. Transfer was limited by the presence of a functional restriction-modification system in recipients, thus bias towards kin might be explained by sharing of identical restriction systems. Such conjugation within lineages sets the stage for longer-term pair-wise coevolutionary interactions between plasmids and bacterial hosts.
Abstract.
Dimitriu T, Souissi W, Morwool P, Darby A, Crickmore N, Raymond B (In Press). Re-inventing pathogen passage for social microbes.
Abstract:
Re-inventing pathogen passage for social microbes
AbstractPassage experiments that sequentially infect hosts with parasites have long been used to manipulate virulence. However, in many invertebrate pathogens passage has been applied naively without a full theoretical understanding of how best to select for increased virulence. This has led to very mixed results. Understanding the evolution of virulence is complex because selection on parasites occurs across multiple spatial scales with potentially different conflicts operating on parasites with different life-histories. For example, in social microbes, strong selection on replication rate within hosts can lead to cheating and loss of virulence, because investment in public goods virulence reduces replication rate. In contrast, selection acting at a between host scale maintains virulence by selecting on parasite population size. In this study we tested how different scales of selection and varying mutation supply affect evolution of virulence against resistant hosts in the specialist insect pathogen Bacillus thuringiensis. aiming to optimize methods for strain improvement against a difficult to kill insect target. We show that selection for infectivity using competition between sub-populations in a metapopulation prevents social cheating, acts to retain key virulence plasmids and facilitates increased virulence. Increased virulence was associated with reduced efficiency of sporulation, and loss of function in putative regulatory genes but not with altered expression of known virulence factors. Selection in a metapopulation provides a broadly applicable tool for improving the efficacy of biocontrol agents. Moreover, a structured host population can facilitate artificial selection on infectivity, while selection on life history traits such as faster replication or larger population sizes can reduce virulence can reduce virulence in social microbes.
Abstract.
Dimitriu T, Misevic D, Capelle JB, Lindner AB, Brown SP, Taddei F (In Press). Selection of horizontal gene transfer through public good production.
Abstract:
Selection of horizontal gene transfer through public good production
AbstractIn bacteria, cooperative genes encoding public good molecules are preferentially located on mobile genetic elements (MGEs), and horizontal transfer of MGEs favours the maintenance of public good cooperation. The rate of horizontal transfer itself can evolve in response to selective pressures acting on both MGEs and bacterial hosts: benefits and costs of infectious spread, but also indirect effects of MGE genes to the host. We show here that carriage of public good genes on MGEs can generate another indirect selection for MGE transfer. Transfer increases public good production and, when relatedness is sufficiently high, public goods benefit preferentially genotypes with high transfer ability. Both our simulations and experiments indicate that transfer is not required to occur among kin, provided that public goods still benefit kin. Public good gene mobility thus aligns the interests of chromosomes and MGEs concerning transfer, promoting gene exchange among bacteria.
Abstract.
2023
Pons BJ, Dimitriu T, Westra ER, van Houte S (2023). Antibiotics that affect translation can antagonize phage infectivity by interfering with the deployment of counter-defenses.
Proc Natl Acad Sci U S A,
120(4).
Abstract:
Antibiotics that affect translation can antagonize phage infectivity by interfering with the deployment of counter-defenses.
It is becoming increasingly clear that antibiotics can both positively and negatively impact the infectivity of bacteriophages (phage), but the underlying mechanisms often remain unclear. Here we demonstrate that antibiotics that target the protein translation machinery can fundamentally alter the outcome of bacteria-phage interactions by interfering with the production of phage-encoded counter-defense proteins. Specifically, using Pseudomonas aeruginosa PA14 and phage DMS3vir as a model, we show that bacteria with Clustered Regularly Interspaced Short Palindromic Repeat, CRISPR associated (CRISPR-Cas) immune systems have elevated levels of immunity against phage that encode anti-CRISPR (acr) genes when translation inhibitors are present in the environment. CRISPR-Cas are highly prevalent defense systems that enable bacteria to detect and destroy phage genomes in a sequence-specific manner. In response, many phages encode acr genes that are expressed immediately following the infection to inhibit key steps of the CRISPR-Cas immune response. Our data show that while phage-carrying acr genes can amplify efficiently on bacteria with CRISPR-Cas immune systems in the absence of antibiotics, the presence of antibiotics that act on protein translation prevents phage amplification, while protecting bacteria from lysis.
Abstract.
Author URL.
Dimitriu T, Souissi W, Morwool P, Darby A, Crickmore N, Raymond B (2023). Selecting for infectivity across metapopulations can increase virulence in the social microbe. <i>Bacillus thuringiensis</i>. Evolutionary Applications, 16(3), 705-720.
2022
Dimitriu T, Kurilovich E, Łapińska U, Severinov K, Pagliara S, Szczelkun MD, Westra ER (2022). Bacteriostatic antibiotics promote CRISPR-Cas adaptive immunity by enabling increased spacer acquisition.
Cell Host Microbe,
30(1), 31-40.e5.
Abstract:
Bacteriostatic antibiotics promote CRISPR-Cas adaptive immunity by enabling increased spacer acquisition.
Phages impose strong selection on bacteria to evolve resistance against viral predation. Bacteria can rapidly evolve phage resistance via receptor mutation or using their CRISPR-Cas adaptive immune systems. Acquisition of CRISPR immunity relies on the insertion of a phage-derived sequence into CRISPR arrays in the bacterial genome. Using Pseudomonas aeruginosa and its phage DMS3vir as a model, we demonstrate that conditions that reduce bacterial growth rates, such as exposure to bacteriostatic antibiotics (which inhibit cell growth without killing), promote the evolution of CRISPR immunity. We demonstrate that this is due to slower phage development under these conditions, which provides more time for cells to acquire phage-derived sequences and mount an immune response. Our data reveal that the speed of phage development is a key determinant of the evolution of CRISPR immunity and suggest that use of bacteriostatic antibiotics can trigger elevated levels of CRISPR immunity in human-associated and natural environments.
Abstract.
Author URL.
Pursey E, Dimitriu T, Paganelli FL, Westra ER, van Houte S (2022). CRISPR-Cas is associated with fewer antibiotic resistance genes in bacterial pathogens.
Philos Trans R Soc Lond B Biol Sci,
377(1842).
Abstract:
CRISPR-Cas is associated with fewer antibiotic resistance genes in bacterial pathogens.
The acquisition of antibiotic resistance (ABR) genes via horizontal gene transfer (HGT) is a key driver of the rise in multidrug resistance amongst bacterial pathogens. Bacterial defence systems per definition restrict the influx of foreign genetic material, and may therefore limit the acquisition of ABR. CRISPR-Cas adaptive immune systems are one of the most prevalent defences in bacteria, found in roughly half of bacterial genomes, but it has remained unclear if and how much they contribute to restricting the spread of ABR. We analysed approximately 40 000 whole genomes comprising the full RefSeq dataset for 11 species of clinically important genera of human pathogens, including Enterococcus, Staphylococcus, Acinetobacter and Pseudomonas. We modelled the association between CRISPR-Cas and indicators of HGT, and found that pathogens with a CRISPR-Cas system were less likely to carry ABR genes than those lacking this defence system. Analysis of the mobile genetic elements (MGEs) targeted by CRISPR-Cas supports a model where this host defence system blocks important vectors of ABR. These results suggest a potential 'immunocompromised' state for multidrug-resistant strains that may be exploited in tailored interventions that rely on MGEs, such as phages or phagemids, to treat infections caused by bacterial pathogens. This article is part of the theme issue 'The secret lives of microbial mobile genetic elements'.
Abstract.
Author URL.
Dimitriu T (2022). Evolution of horizontal transmission in antimicrobial resistance plasmids.
Microbiology (Reading),
168(7).
Abstract:
Evolution of horizontal transmission in antimicrobial resistance plasmids.
Mobile genetic elements (MGEs) are one of the main vectors for the spread of antimicrobial resistance (AMR) across bacteria, due to their ability to move horizontally between bacterial lineages. Horizontal transmission of AMR can increase AMR prevalence at multiple scales, from increasing the prevalence of infections by resistant bacteria to pathogen epidemics and worldwide spread of AMR across species. Among MGEs, conjugative plasmids are the main contributors to the spread of AMR. This review discusses the selective pressures acting on MGEs and their hosts to promote or limit the horizontal transmission of MGEs, the mechanisms by which transmission rates can evolve, and their implications for limiting the spread of AMR, with a focus on AMR plasmids.
Abstract.
Author URL.
2021
Dimitriu T, Misevic D, Lindner AB, Taddei F, Brown SP (2021). Bacteria can be selected to help beneficial plasmids spread.
PLoS Biol,
19(12).
Abstract:
Bacteria can be selected to help beneficial plasmids spread.
A recent commentary raised concerns about aspects of the model and assumptions used in a previous study which demonstrated that selection can favor chromosomal alleles that confer higher plasmid donation rates. Here, the authors of that previous study respond to the concerns raised.
Abstract.
Author URL.
Dimitriu T, Matthews AC, Buckling A (2021). Increased copy number couples the evolution of plasmid horizontal transmission and plasmid-encoded antibiotic resistance.
Abstract:
Increased copy number couples the evolution of plasmid horizontal transmission and plasmid-encoded antibiotic resistance.
Conjugative plasmids are mobile elements which spread horizontally between bacterial hosts, and often confer adaptive phenotypes, including antimicrobial resistance (AMR). Theory suggests that opportunities for horizontal transmission favour plasmids with higher transfer rates, whereas selection for plasmid carriage favour less mobile plasmids. However, little is known about the mechanisms leading to variation in transmission rates in natural plasmids or the resultant effects on their bacterial host. We investigated the evolution of AMR plasmids confronted with different immigration rates of susceptible hosts. Plasmid RP4 did not evolve in response to the manipulations, but plasmid R1 rapidly evolved up to 1000-fold increased transfer rates in the presence of susceptible hosts. Most evolved plasmids also conferred on their hosts the ability to grow at high concentrations of antibiotics. This was because plasmids evolved greater copy numbers, as a function of mutations in the copA gene controlling plasmid replication, causing both higher transfer rates and AMR. Reciprocally, plasmids with increased conjugation rates also evolved when selecting for high levels of AMR, despite the absence of susceptible hosts. Such correlated selection between plasmid transfer and AMR could increase the spread of AMR within populations and communities.
Abstract.
2020
Dimitriu T, Szczelkun MD, Westra ER (2020). Evolutionary Ecology and Interplay of Prokaryotic Innate and Adaptive Immune Systems. Current Biology, 30(19), R1189-R1202.
2019
Dimitriu T, Marchant L, Buckling A, Raymond B (2019). Bacteria from natural populations transfer plasmids mostly towards their kin. Proceedings of the Royal Society B: Biological Sciences, 286
Raymond B, Dimitriu T (2019). Negative frequency dependent selection on plasmid carriage and low fitness costs maintain extended spectrum β-lactamases in Escherichia coli.
Abstract:
Negative frequency dependent selection on plasmid carriage and low fitness costs maintain extended spectrum β-lactamases in Escherichia coli.
Plasmids may maintain antibiotic resistance genes in bacterial populations through conjugation, in the absence of direct selection pressure. However, the costs and benefits of conjugation for plasmid and bacterial fitness are not well understood. Using invasion and competition experiments with plasmid mutants we explicitly tested how conjugation contributes to the maintenance of a plasmid bearing a single extended-spectrum ß-lactamase (ESBL) gene (blaCTX-M-14). Surprisingly, conjugation had little impact on overall frequencies, although it imposed a substantial fitness cost. Instead, stability resulted from the plasmid conferring fitness benefits when rare. Frequency dependent fitness did not require a functional blaCTX-M-14 gene, and was independent of culture media. Fitness benefits when rare are associated with the core plasmid backbone but are able to drive up frequencies of antibiotic resistance because fitness burden of the blaCTX-M-14 gene is very low. Negative frequency dependent fitness can contribute to maintaining a stable frequency of resistance genes in the absence of selection pressure from antimicrobials. In addition, persistent, low cost resistance has broad implications for antimicrobial stewardship.
Abstract.
Dimitriu T, Ashby B, Westra ER (2019). Transposition: a CRISPR Way to Get Around.
Current Biology,
29(18), R886-R889.
Abstract:
Transposition: a CRISPR Way to Get Around
CRISPR-Cas systems provide sequence-specific immunity against selfish genetic elements in prokaryotes. Now, two studies show that transposon-encoded variants can guide sequence-specific transposition. These findings have important practical implications but also raise questions of why and how this strategy would benefit transposons.
Abstract.
2016
Medaney F, Dimitriu T, Ellis RJ, Raymond B (2016). Live to cheat another day: Bacterial dormancy facilitates the social exploitation of β-lactamases.
ISME Journal,
10(3), 778-787.
Abstract:
Live to cheat another day: Bacterial dormancy facilitates the social exploitation of β-lactamases
The breakdown of antibiotics by β-lactamases may be cooperative, since resistant cells can detoxify their environment and facilitate the growth of susceptible neighbours. However, previous studies of this phenomenon have used artificial bacterial vectors or engineered bacteria to increase the secretion of β-lactamases from cells. Here, we investigated whether a broad-spectrum β-lactamase gene carried by a naturally occurring plasmid (pCT) is cooperative under a range of conditions. In ordinary batch culture on solid media, there was little or no evidence that resistant bacteria could protect susceptible cells from ampicillin, although resistant colonies could locally detoxify this growth medium. However, when susceptible cells were inoculated at high densities, late-appearing phenotypically susceptible bacteria grew in the vicinity of resistant colonies. We infer that persisters, cells that have survived antibiotics by undergoing a period of dormancy, founded these satellite colonies. The number of persister colonies was positively correlated with the density of resistant colonies and increased as antibiotic concentrations decreased. We argue that detoxification can be cooperative under a limited range of conditions: if the toxins are bacteriostatic rather than bacteridical; or if susceptible cells invade communities after resistant bacteria; or if dormancy allows susceptible cells to avoid bactericides. Resistance and tolerance were previously thought to be independent solutions for surviving antibiotics. Here, we show that these are interacting strategies: the presence of bacteria adopting one solution can have substantial effects on the fitness of their neighbours.
Abstract.
2015
Dimitriu T, Misevic D, Lindner AB, Taddei F (2015). Mobile genetic elements are involved in bacterial sociality.
Mob Genet Elements,
5(1), 7-11.
Abstract:
Mobile genetic elements are involved in bacterial sociality.
Mobile genetic elements in bacteria are enriched in genes participating in social behaviors, suggesting an evolutionary link between gene mobility and social evolution. Cooperative behaviors, like the production of secreted public good molecules, are susceptible to the invasion of non-cooperative individuals, and their evolutionary maintenance requires mechanisms ensuring that benefits are directed preferentially to cooperators. In order to investigate the reasons for the mobility of public good genes, we designed a synthetic bacterial system where we control and quantify the transfer of public good production genes. In our recent study, we have experimentally shown that horizontal transfer helps maintain public good production in the face of both non-producer organisms and non-producer plasmids. Transfer spreads genes to neighboring cells, thus increasing relatedness and directing a higher proportion of public good benefits to producers. The effect is the strongest when public good genes undergo epidemics dynamics, making horizontal transfer especially relevant for pathogenic bacteria that repeatedly infect new hosts and base their virulence on costly public goods. The promotion of cooperation may be a general consequence of horizontal gene transfer in prokaryotes. Our work has an intriguing parallel, cultural transmission, where horizontal transfer, such as teaching, may preferentially promote cooperative behaviors.
Abstract.
Author URL.
2014
Dimitriu T, Lotton C, Beńard-Capelle J, Misevic D, Brown SP, Lindner AB, Taddei F (2014). Genetic information transfer promotes cooperation in bacteria.
Proceedings of the National Academy of Sciences of the United States of America,
111(30), 11103-11108.
Abstract:
Genetic information transfer promotes cooperation in bacteria
Many bacterial species are social, producing costly secreted "public good" molecules that enhance the growth of neighboring cells. The genes coding for these cooperative traits are often propagated via mobile genetic elements and can be virulence factors from a biomedical perspective. Here, we present an experimental framework that links genetic information exchange and the selection of cooperative traits. Using simulations and experiments based on a synthetic bacterial system to control public good secretion and plasmid conjugation, we demonstrate that horizontal gene transfer can favor cooperation. In a well-mixed environment, horizontal transfer brings a direct infectious advantage to any gene, regardless of its cooperation properties. However, in a structured population transfer selects specifically for cooperation by increasing the assortment among cooperative alleles. Conjugation allows cooperative alleles to overcome rarity thresholds and invade bacterial populations structured purely by stochastic dilution effects. Our results provide an explanation for the prevalence of cooperative genes on mobile elements, and suggest a previously unidentified benefit of horizontal gene transfer for bacteria.
Abstract.