scholarly journals Experimental Evolution of Interference Competition

2021 ◽  
Vol 12 ◽  
Author(s):  
Florien A. Gorter ◽  
Carolina Tabares-Mafla ◽  
Rees Kassen ◽  
Sijmen E. Schoustra
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Experimental Evolution ◽  
Species Interactions ◽  
Interference Competition ◽  
Toxin Production ◽  
Clinical Isolates ◽  
Term Selection ◽  
Selection Of

The importance of interference competition, where individuals compete through antagonistic traits such as the production of toxins, has long been recognized by ecologists, yet understanding how these types of interactions evolve remains limited. Toxin production is thought to be beneficial when competing with a competitor. Here, we explore if antagonism can evolve by long-term selection of the toxin (pyocin) producing strain Pseudomonas aeruginosa PAO1 in the presence (or absence) of one of three clinical isolates of the same species (Recipient) over ten serial transfers. We find that inhibition decreases in the absence of a recipient. In the presence of a recipient, antagonism evolved to be different depending on the recipient used. Our study shows that the evolution of interference competition by toxins can decrease or increase, experimentally demonstrating the importance of this type of interaction for the evolution of species interactions.

Individuals, hierarchies and processes: towards a more complete evolutionary theory

Paleobiology ◽  
1984 ◽  
Vol 10 (2) ◽  
pp. 146-171 ◽  
Author(s):  
Elisabeth S. Vrba ◽  
Niles Eldredge
Keyword(s):  
Downward Causation ◽  
Species Selection ◽  
Process Selection ◽  
Term Selection ◽  
Hierarchical Levels ◽  
Character Variation ◽  
Long Term Trend ◽  
Interlevel Causation ◽  
Selection Of

Hierarchy is a central phenomenon of life. Yet it does not feature as such in traditional biological theory. The genealogical hierarchy is a nested organization of entities at ascending levels. There are phenomena common to all levels: (1) Entities such as genomic constituents, organisms, demes, and species are individuals. (2) They have aggregate characters (statistics of characters of subparts), but also emergent characters (arising from organization among subparts). Character variation changes by (3) introduction of novelty and (4) sorting by differential birth and death. Causation of introduction and sorting of variation at each level may be (5) upward from lower levels, (6) downward from higher levels, or (7) lodged at the focal level. The term “selection” applies to only one of the possible processes which cause sorting at a focal level. Neo-Darwinian explanations are too narrow, both in the levels (of genotypes and phenotypes) and in the directive process (selection) which are stressed. The acknowledgment of additional, hierarchical phenomena does not usually extend beyond lip service. We urge that interlevel causation should feature centrally in explanatory hypotheses of evolution. For instance, a ready explanation for divergence in populations is “selection of random mutants.” But upward causation from genome dynamics (or downward causation from the hierarchical organism) to the directed introduction of mutants may be more important in a given case. Similarly, a long-term trend is traditionally explained as additive evolution in populations. But sorting among species may be the cardinal factor, and the cause may not be species selection but upward causation from lower levels. A general theory of biology is a theory of hierarchical levels—how they arise and interact. This is a preliminary contribution mainly to the latter question.

scholarly journals Optimum selection intensities in artificial selection programmes: an experimental evaluation

1977 ◽  
Vol 30 (2) ◽  
pp. 115-119 ◽  
Author(s):  
R. Frankham
Keyword(s):  
Experimental Evaluation ◽  
Selection Intensity ◽  
Effective Population ◽  
Term Selection ◽  
Optimum Selection ◽  
Selection For ◽  
Selection Intensities ◽  
Selection Of ◽  
Better Than

SUMMARYAn experimental evaluation of Robertson's (1970) theory concerning optimum intensities of selection for selection of varying durations has been carried out using published results from a long term selection study in Drosophila. Agreement of predicted rankings of treatments with expectations was excellent for low values of t/T (generations/total number scored) but poor for larger values of t/T. This was due to the 20% selection intensity treatments responding worse than expected and the 40% treatments relatively better than expected. Several possible reasons for the discrepancies exist but the most likely explanation is considered to be the greater reduction in effective population size due to selection in treatments with more intense selection.

Seed traits evaluation from long-term selection of kernel oil concentration in a high-oil maize population KYHO

2012 ◽  
Vol 92 (5) ◽  
pp. 857-866
Author(s):  
Wang Hong-Wu ◽  
Hu Hai-Xiao ◽  
Song Tong-Ming ◽  
Chen Shao-Jiang
Keyword(s):  
Protein Content ◽  
Oil Content ◽  
Selective Breeding ◽  
Starch Content ◽  
Term Selection ◽  
Kernel Oil ◽  
Maize Population ◽  
Oil Concentration ◽  
Selection Of

Wang, H.-W., Hu, H.-X., Song, T.-M. and Chen, S.-J. 2012. Seed traits evaluation from long-term selection of kernel oil concentration in a high-oil maize population KYHO. Can. J. Plant Sci. 92: 857–866. A high-oil maize population, KYHO, was developed over 10 generations by selective breeding for increased kernel oil content (KOC). The objectives of this study were to evaluate kernel oil selection effects, and measure the trait changes and genetic variance in the embryo and endosperm. Oil, protein, and starch content in the embryo and endosperm were estimated by near-infrared reflectance spectroscopy (NIRS). Mass and volume of embryo and endosperm were measured. Selective breeding increased embryo oil content (EMOC) and endosperm oil content (ENOC), especially EMOC, which changed from 315.62 g kg−1C0 to 592.54 g kg−1C10, resulting in an increase in total embryo and endosperm oil content (EEOC) from 43.32 g kg−1C0 to 139.95 g kg−1C10. With selection for increase in EEOC, embryo protein content (EMPC) decreased slightly; however, endosperm protein content (ENPC) and total protein content (EEPC) increased significantly. Embryo and endosperm starch content (EMSC and ENSC) and total starch content (EESC) all decreased substantially with selection. One hundred embryo mass (EMM) was not notably changed with selection, but 100 embryo volume (EMV) increased significantly. Mass and volume of endosperm (ENM and ENV) and total mass and volume of embryo and endosperm (EEM and EEV) all decreased significantly with selection, possibly due to markedly decreased starch content. Linear regression analysis indicated with each 1 g kg−1EEOC increase, EMOC, ENOC, ENPC, EEPC, EMM, and EMV increased 2.74 g kg−1, 0.16 g kg−1, 0.38 g kg−1, 0.36 g kg−1, 0.06 g, and 0.20 mL, respectively, and EMPC, EMSC, ENSC, EESC, EEM, ENM, EEV, and ENV decreased 0.04 g kg−1, 1.48 g kg−1, 0.60 g kg−1, 1.09 g kg−1, 1.26 g, 1.32 g, 0.97 g, and 1.17 mL, rspectively.

scholarly journals Characterization of clinical isolates of Pseudomonas aeruginosa heterogeneously resistant to carbapenems

2007 ◽  
Vol 56 (1) ◽  
pp. 66-70 ◽  
Author(s):  
Spyros Pournaras ◽  
Alexandros Ikonomidis ◽  
Antonios Markogiannakis ◽  
Nicholas Spanakis ◽  
Antonios N. Maniatis ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Population Analysis ◽  
Growth Curves ◽  
Clinical Isolates ◽  
Lag Phase ◽  
Carbapenem Resistant ◽  
One Step ◽  
Agar Dilution ◽  
Resistant Mutants ◽  
Selection Of

Fourteen apparently carbapenem-susceptible Pseudomonas aeruginosa clinical isolates that exhibited colonies within the inhibition zone around carbapenem discs were analysed. MICs of carbapenems were determined and the isolates were genotyped by PFGE. Population analysis, one-step selection of carbapenem-resistant mutants and growth curves of progenitors and carbapenem-resistant subpopulations were performed. Agar dilution MICs of imipenem and meropenem ranged from 0.5 to 4 mg l−1 and from 0.25 to 2 mg l−1, respectively. Population analysis confirmed subpopulations that grew in concentrations of up to 18 mg l−1 and 12 mg l−1 of imipenem and meropenem, respectively, at frequencies ranging from 6.9×10−5 to 1.1×10−7, suggesting that they might not be detected by standard agar dilution MIC testing. The minority subpopulations exhibited MICs for imipenem ranging from 10 to 20 mg l−1 and for meropenem from 4 to 14 mg l−1. The one-step 8 mg l−1 selection of imipenem-resistant mutants test showed growth in all isolates at frequencies ranging from 3.8×10−4 to 5.1×10−7. Growth curves revealed a prolonged lag phase and a short exponential phase for the heterogeneous subpopulations compared with their respective native subpopulations. These findings may be indicative that the use of carbapenems can lead to selection of P. aeruginosa resistant subpopulations that subsequently cause infections and result in treatment failure.

scholarly journals A large-scale comparison shows that genetic changes causing antibiotic resistance in experimentally evolved Pseudomonas aeruginosa predict those in naturally evolved bacteria

2019 ◽  
Author(s):  
Samuel J. T. Wardell ◽  
Attika Rehman ◽  
Lois W. Martin ◽  
Craig Winstanley ◽  
Wayne M. Patrick ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Experimental Evolution ◽  
Large Scale ◽  
Genetic Basis ◽  
Clinical Isolates ◽  
Resistant Bacteria ◽  
Antibiotic Resistant ◽  
Health Crisis ◽  
Wide Range

AbstractPseudomonas aeruginosa is an opportunistic pathogen that causes a wide range of acute and chronic infections. An increasing number of isolates have acquired mutations that make them antibiotic resistant, making treatment more difficult. To identify resistance-associated mutations we experimentally evolved the antibiotic sensitive strain P. aeruginosa PAO1 to become resistant to three widely used anti-pseudomonal antibiotics, ciprofloxacin, meropenem and tobramycin. Mutants were able to tolerate up to 2048-fold higher concentrations of antibiotic than strain PAO1. Genome sequences were determined for thirteen mutants for each antibiotic. Each mutant had between 2 and 8 mutations. There were at least 8 genes mutated in more than one mutant per antibiotic, demonstrating the complexity of the genetic basis of resistance. Additionally, large deletions of up to 479kb arose in multiple meropenem resistant mutants. For all three antibiotics mutations arose in genes known to be associated with resistance, but also in genes not previously associated with resistance. To determine the clinical relevance of mutations uncovered in experimentally-evolved mutants we analysed the corresponding genes in 457 isolates of P. aeruginosa from patients with cystic fibrosis or bronchiectasis as well as 172 isolates from the general environment. Many of the genes identified through experimental evolution had changes predicted to be function-altering in clinical isolates but not in isolates from the general environment, showing that mutated genes in experimentally evolved bacteria can predict those that undergo mutation during infection. These findings expand understanding of the genetic basis of antibiotic resistance in P. aeruginosa as well as demonstrating the validity of experimental evolution in identifying clinically-relevant resistance-associated mutations.ImportanceThe rise in antibiotic resistant bacteria represents an impending global health crisis. As such, understanding the genetic mechanisms underpinning this resistance can be a crucial piece of the puzzle to combatting it. The importance of this research is that by experimentally evolving P. aeruginosa to three clinically relevant antibiotics, we have generated a catalogue of genes that can contribute to resistance in vitro. We show that many (but not all) of these genes are clinically relevant, by identifying variants in clinical isolates of P. aeruginosa. This research furthers our understanding of the genetics leading to resistance in P. aeruginosa and provides tangible evidence that these genes can play a role clinically, potentially leading to new druggable targets or inform therapies.

scholarly journals A Large-Scale Whole-Genome Comparison Shows that Experimental Evolution in Response to Antibiotics Predicts Changes in Naturally Evolved Clinical Pseudomonas aeruginosa

2019 ◽  
Vol 63 (12) ◽  
Author(s):  
Samuel J. T. Wardell ◽  
Attika Rehman ◽  
Lois W. Martin ◽  
Craig Winstanley ◽  
Wayne M. Patrick ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Experimental Evolution ◽  
Large Scale ◽  
Opportunistic Pathogen ◽  
Clinical Isolates ◽  
Genome Comparison ◽  
Chronic Infections ◽  
Content Type ◽  
Large Deletions ◽  
Wide Range

ABSTRACT Pseudomonas aeruginosa is an opportunistic pathogen that causes a wide range of acute and chronic infections. An increasing number of isolates have mutations that make them antibiotic resistant, making treatment difficult. To identify resistance-associated mutations, we experimentally evolved the antibiotic-sensitive strain P. aeruginosa PAO1 to become resistant to three widely used antipseudomonal antibiotics, namely, ciprofloxacin, meropenem, and tobramycin. Mutants could tolerate up to 2,048-fold higher concentrations of antibiotics than strain PAO1. Genome sequences were determined for 13 mutants for each antibiotic. Each mutant had between 2 and 8 mutations. For each antibiotic, at least 8 genes were mutated in multiple mutants, demonstrating the genetic complexity of resistance. For all three antibiotics, mutations arose in genes known to be associated with resistance but also in genes not previously associated with resistance. To determine the clinical relevance of mutations uncovered in this study, we analyzed the corresponding genes in 558 isolates of P. aeruginosa from patients with chronic lung disease and in 172 isolates from the general environment. Many genes identified through experimental evolution had predicted function-altering changes in clinical isolates but not in environmental isolates, showing that mutated genes in experimentally evolved bacteria can predict those that undergo mutation during infection. Additionally, large deletions of up to 479 kb arose in experimentally evolved meropenem-resistant mutants, and large deletions were present in 87 of the clinical isolates. These findings significantly advance understanding of antibiotic resistance in P. aeruginosa and demonstrate the validity of experimental evolution in identifying clinically relevant resistance-associated mutations.

scholarly journals The Central Role of PDR1 in the Foundation of Yeast Drug Resistance

2006 ◽  
Vol 282 (7) ◽  
pp. 5063-5074 ◽  
Author(s):  
Vivienne Fardeau ◽  
Gaëlle Lelandais ◽  
Andrew Oldfield ◽  
Hélène Salin ◽  
Sophie Lemoine ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Genetic Determinants ◽  
Term Selection ◽  
Basal Expression ◽  
Drug Dependent ◽  
Dna Binding Properties ◽  
Early Drug ◽  
Selection Of

The widespread pleiotropic drug resistance (PDR) phenomenon is well described as the long term selection of genetic variants expressing constitutively high levels of membrane transporters involved in drug efflux. However, the transcriptional cascades leading to the PDR phenotype in wild-type cells are largely unknown, and the first steps of this phenomenon are poorly understood. We investigated the transcriptional mechanisms underlying the establishment of an efficient PDR response in budding yeast. We show that within a few minutes of drug sensing yeast elicits an effective PDR response, involving tens of PDR genes. This early PDR response (ePDR) is highly dependent on the Pdr1p transcription factor, which is also one of the major genetic determinants of long term PDR acquisition. The activity of Pdr1p in early drug response is not drug-specific, as two chemically unrelated drugs, benomyl and fluphenazine, elicit identical, Pdr1p-dependent, ePDR patterns. Our data also demonstrate that Pdr1p is an original stress response factor, the DNA binding properties of which do not depend on the presence of drugs. Thus, Pdr1p is a promoter-resident regulator involved in both basal expression and rapid drug-dependent induction of PDR genes.

scholarly journals Adaptive Interactions of Achromobacter spp. with Pseudomonas aeruginosa in Cystic Fibrosis Chronic Lung Co-Infection

Pathogens ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 978
Author(s):  
Angela Sandri ◽  
Janus Anders Juul Haagensen ◽  
Laura Veschetti ◽  
Helle Krogh Johansen ◽  
Søren Molin ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Species Interactions ◽  
Biofilm Formation ◽  
Emerging Pathogens ◽  
Adhesion Ability ◽  
Long Time ◽  
Achromobacter Sp ◽  
Longitudinal Strains

In the lungs of patients with cystic fibrosis (CF), the main pathogen Pseudomonas aeruginosa is often co-isolated with other microbes, likely engaging in inter-species interactions. In the case of chronic co-infections, this cohabitation can last for a long time and evolve over time, potentially contributing to the clinical outcome. Interactions involving the emerging pathogens Achromobacter spp. have only rarely been studied, reporting inhibition of P. aeruginosa biofilm formation. To evaluate the possible evolution of such interplay, we assessed the ability of Achromobacter spp. isolates to affect the biofilm formation of co-isolated P. aeruginosa strains during long-term chronic co-infections. We observed both competition and cohabitation. An Achromobacter sp. isolate secreted exoproducts interfering with the adhesion ability of a co-isolated P. aeruginosa strain and affected its biofilm formation. Conversely, a clonal Achromobacter sp. strain later isolated from the same patient, as well as two longitudinal strains from another patient, did not show similar competitive behavior against its P. aeruginosa co-isolates. Genetic variants supporting the higher virulence of the competitive Achromobacter sp. isolate were found in its genome. Our results confirm that both inter-species competition and cohabitation are represented during chronic co-infections in CF airways, and evolution of these interplays can happen even at the late stages of chronic infection.

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