Specific phenotypic, genomic, and fitness evolutionary trajectories toward antibiotic resistance induced by pesticide co-stressors in Escherichia coli

To explore how co-occurring non-antibiotic environmental stressors affect evolutionary trajectories toward antibiotic resistance, we exposed susceptible Escherichia coli K-12 populations to environmentally relevant levels of pesticides and streptomycin for 500 generations. The coexposure substantially changed the phenotypic, genotypic, and fitness evolution trajectories, resulting in much stronger streptomycin resistance (>15-fold increase) of the populations. Antibiotic target modification mutations in rpsL and rsmG, which emerged and dominated at late stages of evolution, conferred the strong resistance even with less than 1% abundance, while the off-target mutations in nuoG, nuoL, glnE, and yaiW dominated at early stages only led to mild resistance (2.5 ~ 6-fold increase). Moreover, the strongly resistant mutants exhibited lower fitness costs even without the selective pressure and had lower minimal selection concentrations than the mildly resistant ones. Removal of the selective pressure did not reverse the strong resistance of coexposed populations at a later evolutionary stage. The findings suggest higher risks of the selection and propagation of strong antibiotic resistance in environments potentially impacted by antibiotics and pesticides.

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Specific phenotypic, genomic, and fitness evolutionary trajectories toward streptomycin resistance induced by pesticide co-stressors in Escherichia coli

ISME Communications ◽

10.1038/s43705-021-00041-z ◽

2021 ◽

Vol 1 (1) ◽

Author(s):

Yue Xing ◽

Xiaoxi Kang ◽

Siwei Zhang ◽

Yujie Men

Keyword(s):

Escherichia Coli ◽

Antibiotic Resistance ◽

Selective Pressure ◽

Fold Increase ◽

Streptomycin Resistance ◽

Evolutionary Stage ◽

Fitness Costs ◽

Evolutionary Trajectories ◽

K 12 ◽

Late Stages

AbstractTo explore how co-occurring non-antibiotic environmental stressors affect evolutionary trajectories toward antibiotic resistance, we exposed susceptible Escherichia coli K-12 populations to environmentally relevant levels of pesticides and streptomycin for 500 generations. The coexposure substantially changed the phenotypic, genotypic, and fitness evolutionary trajectories, resulting in much stronger streptomycin resistance (>15-fold increase) of the populations. Antibiotic target modification mutations in rpsL and rsmG, which emerged and dominated at late stages of evolution, conferred the strong resistance even with less than 1% abundance, while the off-target mutations in nuoG, nuoL, glnE, and yaiW dominated at early stages only led to mild resistance (2.5–6-fold increase). Moreover, the strongly resistant mutants exhibited lower fitness costs even without the selective pressure and had lower minimal selection concentrations than the mildly resistant ones. Removal of the selective pressure did not reverse the strong resistance of coexposed populations at a later evolutionary stage. The findings suggest higher risks of the selection and propagation of strong antibiotic resistance in environments potentially impacted by antibiotics and pesticides.

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Explanations accounting for transduction by bacteriophage λ in maltose negative bacteriophage λ resistant mutants of Escherichia coli K-12

MGG Molecular & General Genetics ◽

10.1007/bf00270887 ◽

1978 ◽

Vol 159 (2) ◽

pp. 143-149 ◽

Cited By ~ 12

Author(s):

C. Braun-Breton ◽

M. Hofnung

Keyword(s):

Escherichia Coli ◽

Bacteriophage Λ ◽

Resistant Mutants ◽

K 12

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Cell-Wall Lipopolysaccharides of Ampicillin-Resistant Mutants of Escherichia coli K-12

European Journal of Biochemistry ◽

10.1111/j.1432-1033.1976.tb10526.x ◽

1976 ◽

Vol 66 (2) ◽

pp. 369-377 ◽

Cited By ~ 60

Author(s):

Peter PREHM ◽

Stephan STIRM ◽

Barbara JANN ◽

Klaus JANN ◽

Hans G. BOMAN

Keyword(s):

Escherichia Coli ◽

Cell Wall ◽

Resistant Mutants ◽

K 12

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Potentiation by L-cysteine of the bactericidal effect of hydrogen peroxide in Escherichia coli

Journal of Bacteriology ◽

10.1128/jb.152.1.81-88.1982 ◽

1982 ◽

Vol 152 (1) ◽

pp. 81-88

Author(s):

E H Berglin ◽

M B Edlund ◽

G K Nyberg ◽

J Carlsson

Keyword(s):

Escherichia Coli ◽

Hydrogen Peroxide ◽

Metal Ion ◽

Chelating Agent ◽

Fold Increase ◽

Bactericidal Effect ◽

Anaerobic Conditions ◽

Dna Breakage ◽

E Coli ◽

K 12

Under anaerobic conditions an exponentially growing culture of Escherichia coli K-12 was exposed to hydrogen peroxide in the presence of various compounds. Hydrogen peroxide (0.1 mM) together with 0.1 mM L-cysteine or L-cystine killed the organisms more rapidly than 10 mM hydrogen peroxide alone. The exposure of E. coli to hydrogen peroxide in the presence of L-cysteine inhibited some of the catalase. This inhibition, however, could not fully explain the 100-fold increase in hydrogen peroxide sensitivity of the organism in the presence of L-cysteine. Of other compounds tested only some thiols potentiated the bactericidal effect of hydrogen peroxide. These thiols were effective, however, only at concentrations significantly higher than 0.1 mM. The effect of L-cysteine and L-cystine could be annihilated by the metal ion chelating agent 2,2'-bipyridyl. DNA breakage in E. coli K-12 was demonstrated under conditions where the organisms were killed by hydrogen peroxide.

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YdgG (TqsA) Controls Biofilm Formation in Escherichia coli K-12 through Autoinducer 2 Transport

Journal of Bacteriology ◽

10.1128/jb.188.2.587-598.2006 ◽

2006 ◽

Vol 188 (2) ◽

pp. 587-598 ◽

Cited By ~ 128

Author(s):

Moshe Herzberg ◽

Ian K. Kaye ◽

Wolfgang Peti ◽

Thomas K. Wood

Keyword(s):

Escherichia Coli ◽

Biofilm Formation ◽

Acid Production ◽

Polysialic Acid ◽

Fold Increase ◽

Uncharacterized Protein ◽

Biofilm Thickness ◽

Autoinducer 2 ◽

Membrane Spanning ◽

K 12

ABSTRACT YdgG is an uncharacterized protein that is induced in Escherichia coli biofilms. Here it is shown that deletion of ydgG decreased extracellular and increased intracellular concentrations of autoinducer 2 (AI-2); hence, YdgG enhances transport of AI-2. Consistent with this hypothesis, deletion of ydgG resulted in a 7,000-fold increase in biofilm thickness and 574-fold increase in biomass in flow cells. Also consistent with the hypothesis, deletion of ydgG increased cell motility by increasing transcription of flagellar genes (genes induced by AI-2). By expressing ydgG in trans, the wild-type phenotypes for extracellular AI-2 activity, motility, and biofilm formation were restored. YdgG is also predicted to be a membrane-spanning protein that is conserved in many bacteria, and it influences resistance to several antimicrobials, including crystal violet and streptomycin (this phenotype could also be complemented). Deletion of ydgG also caused 31% of the bacterial chromosome to be differentially expressed in biofilms, as expected, since AI-2 controls hundreds of genes. YdgG was found to negatively modulate expression of flagellum- and motility-related genes, as well as other known products essential for biofilm formation, including operons for type 1 fimbriae, autotransporter protein Ag43, curli production, colanic acid production, and production of polysaccharide adhesin. Eighty genes not previously related to biofilm formation were also identified, including those that encode transport proteins (yihN and yihP), polysialic acid production (gutM and gutQ), CP4-57 prophage functions (yfjR and alpA), methionine biosynthesis (metR), biotin and thiamine biosynthesis (bioF and thiDFH), anaerobic metabolism (focB, hyfACDR, ttdA, and fumB), and proteins with unknown function (ybfG, yceO, yjhQ, and yjbE); 10 of these genes were verified through mutation to decrease biofilm formation by 40% or more (yfjR, bioF, yccW, yjbE, yceO, ttdA, fumB, yjiP, gutQ, and yihR). Hence, it appears YdgG controls the transport of the quorum-sensing signal AI-2, and so we suggest the gene name tqsA.

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Antibiotic breakdown by susceptible bacteria enhances the establishment of β-lactam resistant mutants

10.1101/2021.04.20.440616 ◽

2021 ◽

Author(s):

Manja Saebelfeld ◽

Suman G Das ◽

Jorn Brink ◽

Arno Hagenbeek ◽

Joachim Krug ◽

...

Keyword(s):

Escherichia Coli ◽

Antibiotic Resistance ◽

Theoretical Model ◽

Enzymatic Activity ◽

Social Interactions ◽

Single Cells ◽

Antibiotic Concentration ◽

High Frequencies ◽

Establishment Probability ◽

Resistant Mutants

For a better understanding of the evolution of antibiotic resistance, it is imperative to study the factors that determine the initial establishment of mutant resistance alleles. In addition to the antibiotic concentration, the establishment of resistance alleles may be affected by interactions with the surrounding susceptible cells from which they derive, for instance via the release of nutrients or removal of the antibiotic. Here, we investigate the effects of social interactions with surrounding susceptible cells on the establishment of Escherichia coli mutants with increasing β-lactamase activity (i.e. the capacity to hydrolyze β-lactam antibiotics) from single cells under the exposure of the antibiotic cefotaxime on agar plates. We find that mutant establishment probability is increased in the presence of susceptible cells due to the active breakdown of the antibiotic, but the rate of breakdown by the susceptible strain is much higher than expected based on its low enzymatic activity. A detailed theoretical model suggests that this observation can be explained by cell filamentation causing delayed lysis. While susceptible cells may hamper the spread of higher-resistant β-lactamase mutants at relatively high frequencies, our findings show that they could promote establishment during their emergence.

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Increased Survival of Antibiotic-Resistant Escherichia coli inside Macrophages

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.01632-12 ◽

2012 ◽

Vol 57 (1) ◽

pp. 189-195 ◽

Cited By ~ 33

Author(s):

Migla Miskinyte ◽

Isabel Gordo

Keyword(s):

Escherichia Coli ◽

Antibiotic Resistance ◽

Bacterial Infections ◽

Resistance Mutation ◽

Fitness Cost ◽

Resistance Mutations ◽

Content Type ◽

E Coli ◽

Fitness Effects ◽

K 12

ABSTRACTMutations causing antibiotic resistance usually incur a fitness cost in the absence of antibiotics. The magnitude of such costs is known to vary with the environment. Little is known about the fitness effects of antibiotic resistance mutations when bacteria confront the host's immune system. Here, we study the fitness effects of mutations in therpoB,rpsL, andgyrAgenes, which confer resistance to rifampin, streptomycin, and nalidixic acid, respectively. These antibiotics are frequently used in the treatment of bacterial infections. We measured two important fitness traits—growth rate and survival ability—of 12Escherichia coliK-12 strains, each carrying a single resistance mutation, in the presence of macrophages. Strikingly, we found that 67% of the mutants survived better than the susceptible bacteria in the intracellular niche of the phagocytic cells. In particular, allE. colistreptomycin-resistant mutants exhibited an intracellular advantage. On the other hand, 42% of the mutants incurred a high fitness cost when the bacteria were allowed to divide outside of macrophages. This study shows that single nonsynonymous changes affecting fundamental processes in the cell can contribute to prolonged survival ofE. coliin the context of an infection.

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Identification in various chlorate-resistant mutants of a protein involved in the activation of nitrate reductase in the soluble fraction of a chlA mutant of Escherichia coli K-12

Biochimica et Biophysica Acta (BBA) - General Subjects ◽

10.1016/0304-4165(85)90035-2 ◽

1985 ◽

Vol 839 (2) ◽

pp. 181-190 ◽

Cited By ~ 7

Author(s):

G GIORDANO ◽

L SARACINO ◽

L GRILLET

Keyword(s):

Escherichia Coli ◽

Nitrate Reductase ◽

Soluble Fraction ◽

Resistant Mutants ◽

K 12

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Aromatic Acid Metabolites of Escherichia coli K-12 Can Induce the marRAB Operon

Journal of Bacteriology ◽

10.1128/jb.00371-10 ◽

2010 ◽

Vol 192 (18) ◽

pp. 4786-4789 ◽

Cited By ~ 29

Author(s):

Lon M. Chubiz ◽

Christopher V. Rao

Keyword(s):

Escherichia Coli ◽

Antibiotic Resistance ◽

Stress Tolerance ◽

Aromatic Acid ◽

Tryptophan Biosynthesis ◽

Metabolic Intermediates ◽

Acid Metabolites ◽

K 12 ◽

Solvent Stress

ABSTRACT MarR is a key regulator of the marRAB operon involved in antibiotic resistance and solvent stress tolerance in Escherichia coli. We show that two metabolic intermediates, 2,3-dihydroxybenzoate and anthranilate, involved in enterobactin and tryptophan biosynthesis, respectively, can activate marRAB transcription. We also found that a third intermediate involved in ubiquinone biosynthesis, 4-hydroxybenzoate, activates marRAB transcription in the absence of TolC. Of the three, however, only 2,3-dihydroxybenzoate directly binds MarR and affects its activity.

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