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646 results for “Pseudomonas aeruginosa”
Data from: Spite versus cheats: competition among social strategies shapes virulence in Pseudomonas aeruginosa
Social interactions have been shown to play an important role in bacterial evolution and virulence. The majority of empirical studies conducted have only considered social traits in isolation, yet numerous social traits, such as the production of spiteful bacteriocins (anti-competitor toxins) and iron-scavenging siderophores (a public good) by the opportunistic pathogen Pseudomonas aeruginosa, are frequently expressed simultaneously. Crucially, both bacteriocin production and siderophore cheating can be favoured under the same competitive conditions, and we develop theory and carry out experiments to determine how the success of a bacteriocin-producing genotype is influenced by social cheating of susceptible competitors and the resultant impact on disease severity (virulence). Consistent with our theoretical predictions, we find that the spiteful genotype is favoured at higher local frequencies when competing against public good cheats. Furthermore, the relationship between spite frequency and virulence is significantly altered when the spiteful genotype is competed against cheats compared with cooperators. These results confirm the ecological and evolutionary importance of considering multiple social traits simultaneously. Moreover, our results are consistent with recent theory regarding the invasion conditions for strong reciprocity (helping cooperators and harming non-cooperators).
Data from: Social evolution of toxic metal bioremediation in Pseudomonas aeruginosa.
Bacteria are often iron-limited, and hence produce extracellular iron-scavenging siderophores. A crucial feature of siderophore production is that it can be an altruistic behaviour (individually costly but benefitting neighbouring cells), thus siderophore producers can be invaded by non-producing social 'cheats'. Recent studies have shown that siderophores can also bind other heavy metals (such as Cu and Zn), but in this case siderophore chelation actually reduces metal uptake by bacteria. These complexes reduce heavy metal toxicity, hence siderophore production may contribute to toxic metal bioremediation. Here, we show that siderophore production in the context of bioremediation is also an altruistic trait and can be exploited by cheating phenotypes in the opportunistic pathogen Pseudomonas aeruginosa. Specifically, we show that in toxic copper concentrations (i) siderophore non-producers evolve de novo and reach high frequencies, and (ii) producing strains are fitter than isogenic non-producing strains in monoculture, and vice versa in co-culture. Moreover, we show that the evolutionary effect copper has on reducing siderophore production is greater than the reduction observed under iron-limited conditions. We discuss the relevance of these results to the evolution of siderophore production in natural communities and heavy metal bioremediation.
Data from: The bacterium Pseudomonas aeruginosa senses and gradually responds to inter-specific competition for iron
Phenotypic plasticity in response to competition is a well-described phenomenon in higher organisms. Here, we show that also bacteria have the ability to sense the presence of competitors and mount fine-tuned responses to match prevailing levels of competition. In our experiments, we studied inter-specific competition for iron between the bacterium Pseudomonas aeruginosa (PA) and its competitor Burkholderia cenocepacia (BC). We focused on the ability of PA to phenotypically adjust the production of pyoverdine, an iron-scavenging siderophore. We found that PA up-regulates pyoverdine production early on during competition under condition of low iron availability. This plastic upregulation was fine-tuned in response to the level of competition imposed by BC, and seems to confer a relative fitness benefit to PA in the form of an earlier initiation of growth. At later time points, however, PA showed reduced growth in mixed compared to monoculture, suggesting that competitive responses are costly. Altogether, our results demonstrate that phenotypic plasticity in siderophore production plays an important role in inter-specific competition for iron. Upregulating siderophore production may be a powerful strategy to lock iron away from competing species, and to reserve this nutrient for strain members possessing the compatible receptor for uptake.
Data from: Dynamic social behaviour in a bacterium: Pseudomonas aeruginosa partially compensates for siderophore loss to cheats
Cooperation underlies diverse phenomena including the origins of multicellular life, human behaviour in economic markets and the mechanisms by which pathogenic bacteria cause disease. Experiments with microorganisms have advanced our understanding of how, when and why cooperation evolves, but the extent to which microbial cooperation can recapitulate aspects of animal behaviour is debated. For instance, understanding the evolution of behavioural response rules (how should one individual respond to another's decision to cooperate or defect?) is a key part of social evolution theory, but the possible existence of such rules in social microbes has not been explored. In one specific context (biparental care in animals), cooperation is maintained if individuals respond to a partner's defection by increasing their own investment into cooperation, but not so much that this fully compensates for the defector's lack of investment. This is termed 'partial compensation.' Here, I show that partial compensation for the presence of non-cooperating 'cheats' is also observed in a microbial social behaviour: the cooperative production of iron-scavenging siderophores by the bacterium Pseudomonas aeruginosa. A period of evolution in the presence of cheats maintains this response, whereas evolution in the absence of cheats leads to a loss of compensatory behaviour. These results demonstrate i) the remarkable flexibility of bacterial social behaviour; ii) the potential generality of partial compensation as a social response rule; and iii) the need for mathematical models to explore the evolution of response rules in multi-player social interactions.
Data from: Epistasis buffers the fitness effects of rifampicin-resistance mutations in Pseudomonas aeruginosa
Epistatic interactions between resistance mutations in antibiotic-free environments potentially play a crucial role in the spread of resistance in pathogen populations by determining the fitness cost associated with resistance. We used an experimental evolution approach to test for epistatic interactions between 14 different pairs of rifampicin mutations in the pathogenic bacterium Pseudomonas aeruginosa in 42 different rifampicin-free environments. First, we show that epistasis between rifampicin-resistance mutations tends to be antagonistic: the fitness effect of having two mutations is generally smaller than that predicted from the effects of individual mutations on the wild type. Second, we show that sign epistasis between resistance mutations is both common and strong; most notably, pairs of deleterious resistance mutations often partially or completely compensate for each others' costs, revealing a novel mechanism for compensatory adaptation. These results suggest that antagonistic epistasis between intragenic resistance mutations may be a key determinant of the cost of antibiotic resistance and compensatory adaptation in pathogen populations.
Data from: Evolutionary dynamics of interlinked public goods traits: an experimental study of siderophore production in Pseudomonas aeruginosa
Public goods cooperation is common in microbes, and there is much interest in understanding how such traits evolve. Research in recent years has identified several important factors that shape the evolutionary dynamics of such systems, yet few studies have investigated scenarios involving interactions between multiple public goods. Here we offer general predictions about the evolutionary trajectories of two public goods traits having positive, negative or neutral regulatory influence on one another's expression, and we report on a test of some of our predictions in the context of Pseudomonas aeruginosa's production of two interlinked iron-scavenging siderophores. First, we confirmed that both pyoverdine and pyochelin siderophores do operate as public goods under appropriate environmental conditions. We then tracked their production in lines experimentally evolved under different iron-limitation regimes known to favour different siderophore expression profiles. Under strong iron limitation, where pyoverdine represses pyochelin, we saw a decline in pyoverdine and a concomitant increase in pyochelin – consistent with expansion of pyoverdine-defective cheats derepressed for pyochelin. Under moderate iron limitation, pyochelin declined – again consistent with an expected cheat invasion scenario – but there was no concomitant shift in pyoverdine because cross-suppression between the traits is unidirectional only. Alternating exposure to strong and moderate iron-limitation caused qualitatively similar though lesser shifts compared to the constant-environment regimes. Our results confirm that the regulatory inter-connections between public goods traits can significantly modulate the course of evolution, yet also suggest how we can start to predict the impacts such complexities will have on phenotypic divergence and community stability.
Data from: Selection experiments reveal trade-offs between swimming and twitching motilities in Pseudomonas aeruginosa
Bacteria possess a range of mechanisms to move in different environments, and these mechanisms have important direct and correlated impacts on the virulence of opportunistic pathogens. Bacteria use two surface organelles to facilitate motility: a single polar flagellum, and type IV pili, enabling swimming in aqueous habitats and twitching along hard surfaces, respectively. Here, we address whether there are trade-offs between these motility mechanisms, and hence whether different environments could select for altered motility. We experimentally evolved initially isogenic Pseudomonas aeruginosa under conditions which favoured the different types of motility, and found evidence for a trade-off mediated by antagonistic pleiotropy between swimming and twitching. Moreover, changes in motility resulted in correlated changes in other behaviours, including biofilm formation and growth within an insect host. This suggests environmental origins of a particular motile opportunistic pathogen could predictably influence motility and virulence.
Data from: Linking system-wide impacts of RNA polymerase mutations to the fitness cost of rifampin resistance in Pseudomonas aeruginosa
Fitness costs play a key role in the evolutionary dynamics of antibiotic resistance in bacteria by generating selection against resistance in the absence of antibiotics. Although the genetic basis of antibiotic resistance is well understood, the precise molecular mechanisms linking the genetic basis of resistance to its fitness cost remain poorly characterized. Here, we examine how the system-wide impacts of mutations in the RNA polymerase (RNAP) gene rpoB shape the fitness cost of rifampin resistance in Pseudomonas aeruginosa. Rifampin resistance mutations reduce transcriptional efficiency, and this explains 76% of the variation in fitness among rpoB mutants. The pleiotropic consequence of rpoB mutations is that mutants show altered relative transcript levels of essential genes. We find no evidence that global transcriptional responses have an impact on the fitness cost of rifampin resistance as revealed by transcriptome sequencing (RNA-Seq). Global changes in the transcriptional profiles of rpoB mutants compared to the transcriptional profile of the rifampin-sensitive ancestral strain are subtle, demonstrating that the transcriptional regulatory network of P. aeruginosa is robust to the decreased transcriptional efficiency associated with rpoB mutations. On a smaller scale, we find that rifampin resistance mutations increase the expression of RNAP due to decreased termination at an attenuator upstream from rpoB, and we argue that this helps to minimize the cost of rifampin resistance by buffering against reduced RNAP activity. In summary, our study shows that it is possible to dissect the molecular mechanisms underpinning variation in the cost of rifampin resistance and highlights the importance of genome-wide buffering of relative transcript levels in providing robustness against resistance mutations. IMPORTANCE Antibiotic resistance mutations carry fitness costs. Relative to the characteristics of their antibiotic-sensitive ancestors, resistant mutants show reduced growth rates and competitive abilities. Fitness cost plays an important role in the evolution of antibiotic resistance in the absence of antibiotics; however, the molecular mechanisms underlying these fitness costs is not well understood. We applied a systems-level approach to dissect the molecular underpinnings of the fitness costs associated with rifampin resistance in P. aeruginosa and showed that most of the variation in fitness cost can be explained by the direct effect of resistance mutations on the enzymatic activity of the mutated gene. Pleiotropic changes in transcriptional profiles are subtle at a genome-wide scale, suggesting that the gene regulatory network of P. aeruginosa is robust in the face of the direct effects of resistance mutations.
Data from: Co-evolutionary dynamics between public good producers and cheats in the bacterium Pseudomonas aeruginosa
The production of beneficial public goods is common in the microbial world, and so is cheating – the exploitation of public goods by non-producing mutants. Here, we examine co-evolutionary dynamics between cooperators and cheats and ask whether cooperators can evolve strategies to reduce the burden of exploitation, and whether cheats in turn can improve their exploitation abilities. We evolved cooperators of the bacterium Pseudomonas aeruginosa, producing the shareable iron-scavenging siderophore pyoverdine, together with cheats, defective in pyoverdine production but proficient in uptake. We found that cooperators managed to co-exist with cheats in 56% of all replicates over approximately 150 generations of experimental evolution. Growth and competition assays revealed that co-existence was fostered by a combination of general adaptions to the media and specific adaptions to the co-evolving opponent. Phenotypic screening and whole-genome re-sequencing of evolved clones confirmed this pattern, and suggest that cooperators became less exploitable by cheats because they significantly reduced their pyoverdine investment. Cheats, meanwhile, improved exploitation efficiency through mutations blocking the costly pyoverdine-signalling pathway. Moreover, cooperators and cheats evolved reduced motility, a pattern that likely represents adaptation to laboratory conditions, but at the same time also affects social interactions by reducing strain mixing and pyoverdine sharing. Overall, we observed parallel evolution, where co-existence of cooperators and cheats was enabled by a combination of adaptations to the abiotic and social environment and their interactions.
Data from: The path to re-evolve cooperation is constrained in Pseudomonas aeruginosa
Background. A common form of cooperation in bacteria is based on the secretion of beneficial metabolites, shareable as public good among cells within a group. Because cooperation can be exploited by "cheating" mutants, which contribute less or nothing to the public good, there has been great interest in understanding the conditions required for cooperation to remain evolutionarily stable. In contrast, much less is known about whether cheats, once fixed in the population, are able to revert back to cooperation when conditions change. Here, we tackle this question by subjecting experimentally evolved cheats of Pseudomonas aeruginosa, partly deficient for the production of the iron-scavenging public good pyoverdine, to conditions previously shown to favor cooperation. Results. Following approximately 200 generations of experimental evolution, we screened 720 evolved clones for changes in their pyoverdine production levels. We found no evidence for the re-evolution of full cooperation, even in environments with increased spatial structure, and reduced costs of public good production - two conditions that have previously been shown to maintain cooperation. In contrast, we observed selection for complete abolishment of pyoverdine production. The patterns of complete trait degradation were likely driven by "cheating on cheats" in unstructured, iron-limited environments where pyoverdine is important for growth, and selection against a maladaptive trait in iron-rich environments where pyoverdine is superfluous. Conclusions. Our study shows that the path to re-evolve public-goods cooperation can be constrained. While a limitation of the number of mutational targets potentially leading to reversion might be one reason for the observed pattern, an alternative explanation is that the selective conditions required for revertants to spread from rare are much more stringent than those needed to maintain cooperation.
The collapse of cooperation during range expansion of Pseudomonas aeruginosa [Source Data]
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Figure 9 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 9 Results of toxA gene replication in clinical isolates of Pseudomonas aeruginosa. Well 1: marker size 50 bp; Well 2–23: positive samples of size 85 bp; Well 24: negative control; Well 25: positive control of Pseudomonas aeruginosa PTCC 17589.
Figure 8 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 8 Results of Pela gene replication in clinical isolates of Pseudomonas aeruginosa. Well 1: marker size 50 bp; Well 2–23: positive samples of size 148 bp; Well 24: negative control; Well 25: positive control of Pseudomonas aeruginosa PTCC 17589.
Figure 7 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 7 Results of lasR gene replication in clinical isolates of Pseudomonas aeruginosa. Well 1: marker size 50 bp; Well 2–26: positive samples of size 130 bp; Well 27: negative control; Well 28: positive control of Pseudomonas aeruginosa PTCC 17589.
Figure 4 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 4 Results of gyrB gene replication in clinical isolates of Pseudomonas aeruginosa. Well 1: marker size 50 bp; Well 2–26: positive samples of size 222 bp; Well 27: negative control; Well 28: positive control of Pseudomonas aeruginosa PTCC 17589.
Figure 6 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 6 Results of exoT gene replication in clinical isolates of Pseudomonas aeruginosa. Well 1: marker size 50 bp; Well 2–36: positive samples of size 471 bp; Well 37: negative control; Well 38: positive control of Pseudomonas aeruginosa PTCC 17589.
Figure 5 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 5 Results of rhlR gene replication in clinical isolates of Pseudomonas aeruginosa. Well 1: marker size 50 bp; Well 2–26: positive samples of size 133 bp; Well 27: negative control; Well 28: positive control of Pseudomonas aeruginosa PTCC 17589.
Figure 18 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 18 The expression rates of MexB gene in the gold nanoparticles-treated samples and non-treated samples; a significant decrease in gene expression was observed between treated and non-treated samples in comparison with the control group. The G74 gene was used as an internal control.
Figure 15 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 15 Melting curve analysis to ensure the specificity of the amplified fragments of the MexB gene that the measured curves of the gene in all samples are consistent and single-peaked.
Figure 17 from: Dorri K, Modaresi F, Shakibaie MR, Moazamian E (2022) Effect of gold nanoparticles on the expression of efflux pump mexA and mexB genes of Pseudomonas aeruginosa strains by Quantitative real-time PCR. Pharmacia 69(1): 125-133. https://doi.org/10.3897/pharmacia.69.e77608
Figure 17 The expression rates of MexA gene in the gold nanoparticles-treated samples and non-treated samples; a significant decrease in gene expression was observed between treated and non-treated samples in comparison with the control group. The G74 gene was used as an internal control.
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