scholarly journals Corrigendum: PasT of Escherichia coli sustains antibiotic tolerance and aerobic respiration as a bacterial homolog of mitochondrial Coq10

2020 ◽  
Vol 9 (12) ◽  
Keyword(s):  
Escherichia Coli ◽  
Aerobic Respiration ◽  
Antibiotic Tolerance ◽  
Bacterial Homolog

scholarly journals PasT of Escherichia coli sustains antibiotic tolerance and aerobic respiration as a bacterial homolog of mitochondrial Coq10

2020 ◽  
Vol 9 (8) ◽  
Author(s):  
Cinzia Fino ◽  
Martin Vestergaard ◽  
Hanne Ingmer ◽  
Fabien Pierrel ◽  
Kenn Gerdes ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Aerobic Respiration ◽  
Antibiotic Tolerance ◽  
Bacterial Homolog

scholarly journals Robustness analysis of culturing perturbations on Escherichia coli colony biofilm beta-lactam and aminoglycoside antibiotic tolerance

2010 ◽  
Vol 10 (1) ◽  
pp. 185 ◽  
Author(s):  
Trevor R Zuroff ◽  
Hans Bernstein ◽  
Jenna Lloyd-Randolfi ◽  
Lourdes Jimenez-Taracido ◽  
Philip S Stewart ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Robustness Analysis ◽  
Aminoglycoside Antibiotic ◽  
Antibiotic Tolerance ◽  
Beta Lactam

Regulatory O 2 tensions for the synthesis of fermentation products in Escherichia coli and relation to aerobic respiration

1997 ◽  
Vol 168 (4) ◽  
pp. 290-296 ◽  
Author(s):  
Sabine Becker ◽  
Dorina Vlad ◽  
Sylvia Schuster ◽  
Peter Pfeiffer ◽  
G. Unden
Keyword(s):  
Escherichia Coli ◽  
Aerobic Respiration ◽  
Fermentation Products

Relationship of the Escherichia coli TrkA System of Potassium Ion Uptake with the F0F1-ATPase Under Growth Conditions Without Anaerobic or Aerobic Respiration

1998 ◽  
Vol 18 (3) ◽  
pp. 143-154 ◽  
Author(s):  
Armen Trchounian ◽  
Yelena Ohanjanyan ◽  
Karine Bagramyan ◽  
Vitya Vardanian ◽  
Eleonora Zakharyan ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Growth Conditions ◽  
Transport Systems ◽  
Aerobic Respiration ◽  
Anaerobic Conditions ◽  
Intact Cells ◽  
Potassium Ion Uptake ◽  
Relationship Of ◽  
The Relationship

K+ uptake by the Escherichia coli TrkA system is unusual in that it requires both ATP and ΔμH; a relation withH+ circulation through the membrane is thereforesuggested. The relationship of this system with the F0F1-ATPase was studied in intact cells grownunder different conditions. A significant increase of the N,N'-dicyclohexylcarbodiimide(DCCD)-inhibitedH+ efflux through the F0F1 by 5 mMK+, but not by Na+ added into thepotassium-free medium was revealed only in fermenting wild-type orparent cells, that were grown under anaerobic conditions withoutanaerobic or aerobic respiration and with the production of H2. Such an increase disappeared in the Δunc or the trkA mutants that have alteredF0F1 or defective TrkA, respectively. This finding indicates a closed relationship between TrkA andF0F1, with these transport systems beingassociated in a single mechanism that functions as an ATP-driven H+–K+-exchanging pump. ADCCD-inhibited H+–K+-exchangethrough these systems with the fixed stoichiometry of H+and K+ fluxes(2H+/K+) and a higherK+ gradient between the cytoplasm and the externalmedium were also found in these bacteria. They were not observed incells cultured under anaerobic conditions in the presence of nitrate orunder aerobic conditions with respiration and without production of H2. The role of anaerobic or aerobic respiration as adeterminant of the relationship of the TrkA with the F0F1 is postulated. Moreover, an increase of DCCD-inhibited H+ efflux by added K+, aswell as the characteristics of DCCD-sensitiveH+–K+-exchange found in a parentstrain, were lost in the arcA mutant with a defective Arc system, suggesting a repression of enzymes in respiratorypathways. In addition, K+ influx in the latest mutantwas not markedly changed by valinomycin or with temperature. The arcA gene product or the Arc system is proposed to beimplicated in the regulation of the relationship between TrkA and F0F1.

scholarly journals Role of Global Regulators and Nucleotide Metabolism in Antibiotic Tolerance in Escherichia coli

2008 ◽  
Vol 52 (8) ◽  
pp. 2718-2726 ◽  
Author(s):  
Sonja Hansen ◽  
Kim Lewis ◽  
Marin Vulić
Keyword(s):  
Escherichia Coli ◽  
Cell Formation ◽  
Nucleotide Metabolism ◽  
Flavin Mononucleotide ◽  
Formation Mechanisms ◽  
Antibiotic Tolerance ◽  
Persister Cells ◽  
Global Regulators ◽  
Persister Cell

ABSTRACT Bacterial populations produce a small number of persister cells that exhibit multidrug tolerance. Persister cells are largely responsible for the antibiotic recalcitrance of biofilm infections. The mechanism of persister cell formation largely remains unknown due to the challenges in identifying persister genes. We screened an ordered comprehensive library of 3,985 Escherichia coli knockout strains to identify mutants with altered antibiotic tolerance. Stationary-state cultures in 96-well plates were exposed to ofloxacin at a concentration which allows only tolerant persister cells to survive. The persister cell level of each culture was determined. A total of 150 mutants with decreased persistence were identified in the initial screen, and subsequent validation confirmed that neither the growth rate nor the ofloxacin MIC was affected for 10 of them. The genes affected in these strains were dnaJ and dnaK (chaperones), apaH (diadenosine tetraphosphatase), surA (peptidyl-prolyl cis-trans isomerase), fis and hns (global regulators), hnr (response regulator of RpoS), dksA (transcriptional regulator of rRNA transcription), ygfA (5-formyl-tetrahydrofolate cyclo-ligase), and yigB (flavin mononucleotide [FMN] phosphatase). The prominent presence of global regulators among these strains pointed to the likely redundancy of persister cell formation mechanisms: the elimination of a regulator controlling several redundant persister genes would be expected to produce a phenotype. This observation is consistent with previous findings for a possible role of redundant genes such as toxin/antitoxin modules in persister cell formation. ygfA and yigB were of special interest. The mammalian homolog of YgfA (methenyltetrahydrofolate synthetase) catalyzes the conversion of 5-formyl-tetrahydrofolate (THF) into the rapidly degraded 5,10-methenyl-THF, depleting the folate pool. The YigB protein is a phosphatase of FMN which would deplete the pool of this cofactor. Stochastic overexpression of these genes could lead to dormancy and, hence, tolerance by depleting the folate and FMN pools, respectively. Consistent with this scenario, the overexpression of both genes produced increased tolerance to ofloxacin.

scholarly journals Salmonella typhimurium intercepts Escherichia coli signaling to enhance antibiotic tolerance

2013 ◽  
Vol 110 (35) ◽  
pp. 14420-14425 ◽  
Author(s):  
N. M. Vega ◽  
K. R. Allison ◽  
A. N. Samuels ◽  
M. S. Klempner ◽  
J. J. Collins
Keyword(s):  
Escherichia Coli ◽  
Salmonella Typhimurium ◽  
Antibiotic Tolerance
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