Escherichia coli MC1061
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR093105_1.fastq.gz | Fastqsanger.gz | |||
| DRR093105_2.fastq.gz | Fastqsanger.gz | |||
| DRR093106_1.fastq.gz | Fastqsanger.gz | |||
| DRR093106_2.fastq.gz | Fastqsanger.gz | |||
| DRR093107_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 36 |
Similar Datasets
Project description:Persisters represent a small bacterial population that is dormant and that survives under antibiotic treatment without experiencing genetic adaptation. Persisters are also considered one of the major reasons for recalcitrant chronic bacterial infections. Although several mechanisms of persister formation have been proposed, it is not clear how cells enter the dormant state in the presence of antibiotics or how persister cell formation can be effectively controlled. A fatty acid compound, cis-2-decenoic acid, was reported to decrease persister formation as well as revert the dormant cells to a metabolically active state. We reasoned that some fatty acid compounds may be effective in controlling bacterial persistence because they are known to benefit host immune systems. This study investigated persister cell formation by pathogens that were exposed to nine fatty acid compounds during antibiotic treatment. We found that three medium chain unsaturated fatty acid ethyl esters (ethyl trans-2-decenoate, ethyl trans-2-octenoate, and ethyl cis-4-decenoate) decreased the level of Escherichia coli persister formation up to 110-fold when cells were exposed to ciprofloxacin or ampicillin antibiotics. RNA sequencing analysis and gene deletion persister studies elucidated that these fatty acids inhibit bacterial persistence by regulating antitoxin HipB. A similar persister cell reduction was observed for pathogenic E. coli EDL933, Pseudomonas aeruginosa PAO1, and Serratia marcescens ICU2-4 strains. This study demonstrates that fatty acid ethyl esters can be used to disrupt bacterial dormancy to combat persistent infectious diseases.
2018-08-08 | GSE112545 | GEO
Project description:Persisters are cells which evade stresses like antibiotics and which are characterized by reduced metabolism and a lack of genetic alterations required to achieve this state. We showed previously that MqsR and MqsA of Escherichia coli are a toxin-antitoxin pair that influence cell physiology (e.g., biofilm formation and motility) via RNase activity as well as through regulation of toxin CspD. Here, we show that deletion of the mqsRA locus decreases persister cell formation and, consistent with this result, overexpression of MqsR increases persister cell formation. Furthermore, toxins Hha, CspD, and HokA increase persister cell formation. In addition, by overproducing MqsR in a series of isogenic mutants, we show that Hha and CspD are necessary for persister cell formation via MqsR overexpression. Surprisingly, Hfq, a small RNA chaperone, decreases persistence. A whole-transcriptome study shows that Hfq induces transport-related genes (oppA, oppB, oppC, oppD, oppF, and dppA), outer membrane protein-related genes (ybfM and ybfN), toxins (hha), and proteases (clpX, clpP, and lon). Taken together, these results indicate that toxins CspD and Hha influence persister cell formation via MqsR and that Hfq plays an important role in the regulation of persister cell formation via regulation of transport or outer membrane proteins. Strains: E. coli BW25113 K-12 hfq deleted mutant vs. wild-type Medium: LB Culture: Planktonic cell grown OD=0.5, adjusted OD=1.0, and then exposed to 100 ug/mL ampicillin for 2 h.
2009-11-07 | E-GEOD-18852 | biostudies-arrayexpress
Project description:When bacteria are challenged with antimicrobials, small numbers of cells may survive treatment. These so-called persister cells are not mutants, but are a set of phenotypic variants which, after re-growth exhibit the same susceptibility properties as their progenitor populations. The presence of persisters may determine the effective therapeutic dose of antibiotics and account for the intractability of biofilm-related infections. In the current investigation, Escherichia coli persister cells were isolated without prior exposure to antimicrobials, using fluorescence-assisted cell sorting of a strain, labelled with a chromosomal green fluorescent protein marker. Levels of persistence were inversely proportional to fluorescence intensity in the gfp-tagged E. coli population, and separated persister cells showed enhanced expression of two groups of genes located in the e14 and CP4-6 cryptic prophage regions when analysed by DNA microarray.
2013-10-13 | E-MEXP-3511 | biostudies-arrayexpress
Project description:Persisters are cells which evade stresses like antibiotics and which are characterized by reduced metabolism and a lack of genetic alterations required to achieve this state. We showed previously that MqsR and MqsA of Escherichia coli are a toxin-antitoxin pair that influence cell physiology (e.g., biofilm formation and motility) via RNase activity as well as through regulation of toxin CspD. Here, we show that deletion of the mqsRA locus decreases persister cell formation and, consistent with this result, overexpression of MqsR increases persister cell formation. Furthermore, toxins Hha, CspD, and HokA increase persister cell formation. In addition, by overproducing MqsR in a series of isogenic mutants, we show that Hha and CspD are necessary for persister cell formation via MqsR overexpression. Surprisingly, Hfq, a small RNA chaperone, decreases persistence. A whole-transcriptome study shows that Hfq induces transport-related genes (oppA, oppB, oppC, oppD, oppF, and dppA), outer membrane protein-related genes (ybfM and ybfN), toxins (hha), and proteases (clpX, clpP, and lon). Taken together, these results indicate that toxins CspD and Hha influence persister cell formation via MqsR and that Hfq plays an important role in the regulation of persister cell formation via regulation of transport or outer membrane proteins.
2009-11-08 | GSE18852 | GEO
Project description:Urinary tract infections (UTIs) represent a major burden across the population, although key facets of their pathogenesis challenge physicians and investigators alike. Escherichia coli epitomizes these obstacles: this Gram-negative bacterial species is the most prevalent agent of UTIs worldwide and can also colonize the urogenital tract in a phenomenon known as asymptomatic bacteriuria (ASB). Unfortunately, at the level of the organism, the relationship between symptomatic UTI and ASB is poorly defined, confounding our understanding of microbial pathogenesis and strategies for clinical management. Unlike diarrheagenic pathotypes of E. coli, the definition of uropathogenic E. coli (UPEC) remains phenomenologic, without conserved phenotypes and (known) genetic determinants that rigorously distinguish UTI- and ASB-associated strains. This manuscript provides a cross-disciplinary review of the current issues – from interrelated mechanistic and diagnostic perspectives – and describes new opportunities by which clinical resources can be leveraged to overcome molecular challenges. Specifically, we present our work harnessing a large collection of patient-derived isolates to identify features that do (and do not) distinguish UTI- from ASB-associated E. coli strains. Analyses of biofilm formation, previously reported to be higher in ASB strains, revealed extensive phenotypic heterogeneity that did not correlate with symptomatology. However, metabolomic experiments revealed distinct signatures between ASB and cystitis isolates, including species in the purine pathway (previously shown to be critical for intracellular survival during acute infection). Together, these studies demonstrate how large-scale, wild-type approaches can help dissect the physiology of colonization-versus-infection, suggesting that the molecular definition of UPEC may rest at the level of global bacterial metabolism.
2019-08-14 | ST001244 | MetabolomicsWorkbench
Project description:Escherichia coli, the common inhabitant of the mammalian intestine, exhibits considerable intraspecies genomic variation, which has been suggested to reflect adaptation to different ecological niches. Also, regulatory trade-offs, e.g., between catabolic versatility and stress protection, are thought to result in significant physiological differences between strains. For these reasons, the relevance of experimental observations made for âdomesticatedâ E. coli strains with regard to the behaviour of this species in its natural environments is often questioned and frequently doubts are raised on the status of E. coli as a defined species. We therefore investigated the variability of important eco-physiological functions such as carbon substrate uptake and breakdown capabilities as well as stress defence mechanisms in the genomes of commensal and pathogenic E. coli strains. Furthermore, eco-physiological properties of environmental strains were compared to standard laboratory strain K-12 MG1655. Catabolic, stress protection, and carbon- and energy source transport operons showed a very low intraspecies variability in 57 commensal and pathogenic E. coli. Environmental isolates adapted to glucose-limited growth in a similar way as E. coli MG1655, namely by increasing their catabolic flexibility and by inducing high affinity substrate uptake systems. Our results indicate that the major eco-physiological properties are highly conserved in the natural population of E. coli. This questions the proposed dominant role of horizontal gene transfer for niche adaptation. Keywords: comparative genomic hybridisation Standard approach for comparative genomic hybrisisation, 5 environmental strains were analysed on commercial E. coli MG1655 arrays (MWG), for each strains, biological replicates were done (separate LB cultures)
2006-12-04 | E-GEOD-6407 | biostudies-arrayexpress
Project description:Escherichia coli, the common inhabitant of the mammalian intestine, exhibits considerable intraspecies genomic variation, which has been suggested to reflect adaptation to different ecological niches. Also, regulatory trade-offs, e.g., between catabolic versatility and stress protection, are thought to result in significant physiological differences between strains. For these reasons, the relevance of experimental observations made for “domesticated” E. coli strains with regard to the behaviour of this species in its natural environments is often questioned and frequently doubts are raised on the status of E. coli as a defined species. We therefore investigated the variability of important eco-physiological functions such as carbon substrate uptake and breakdown capabilities as well as stress defence mechanisms in the genomes of commensal and pathogenic E. coli strains. Furthermore, eco-physiological properties of environmental strains were compared to standard laboratory strain K-12 MG1655. Catabolic, stress protection, and carbon- and energy source transport operons showed a very low intraspecies variability in 57 commensal and pathogenic E. coli. Environmental isolates adapted to glucose-limited growth in a similar way as E. coli MG1655, namely by increasing their catabolic flexibility and by inducing high affinity substrate uptake systems. Our results indicate that the major eco-physiological properties are highly conserved in the natural population of E. coli. This questions the proposed dominant role of horizontal gene transfer for niche adaptation. Keywords: comparative genomic hybridisation
2006-12-05 | GSE6407 | GEO
Project description:Acetylation of lysine residues is conserved in all three kingdoms; however, its role in prokaryotes is unknown. Here we demonstrate that acetylation enables the reference bacterium Escherichia coli to withstand environmental stress. Specifically, the bacterium reaches higher cell densities and becomes more resistant to heat and oxidative stress when its proteins are acetylated, as shown by deletion of the gene encoding acetyltransferase YfiQ and the gene encoding deacetylase CobB, as well as by overproducing YfiQ and CobB. Furthermore, we show that the increase in oxidative stress resistance with acetylation is due to the induction of catalase activity through enhanced katG expression. We also found that two-component system proteins CpxA, PhoP, UvrY, and BasR are associated with cell catalase activity and may be responsible as the connection between bacterial acetylation and the stress response. This is the first demonstration of a specific environmental role of acetylation in prokaryotes.
2012-06-06 | GSE29803 | GEO
Project description:Microarrays allow us to monitor the change in transcription of every gene in the genome in response to a change in cellular state. We use cDNA microarrays to measure the response of E. coli to 13 different antibiotics and 3 synergistic combinations. Hierarchichal clustering reveals 4 distinct classes of antibiotics distinguished by their modes of action, and allows us to predict the mechanism for promethazine, a drug whose mode of action has not previously been established. The expression profiles of the synergistic combinations exhibit a complex relationship between the two component antibiotics, with similarity to one of the two drugs, as well as a surprising number of new gene responses exhibited by E. coli in response to neither drug alone. The subset of drugs which act in synergy with each other suggests that only very specific combination of mechanisms give rise to synergistic behavior. Keywords: stress response, antibiotic response, synergy
2008-02-12 | GSE10440 | GEO
Project description:RNA polymerase (RNAP) is the key transcription machinery and its interaction with genomic DNA orchestrates gene expression in response to environmental cues. Dynamic interaction and localization between RNAP and nucleoid were observed before and after osmotic stress. Chromatin immunoprecipitation (ChIP) of RNAP β’ subunit together with chromatin profiling by ChIP-on-chip analysis demonstrated the dynamics of genome-wide RNAP-DNA interactions during osmotic stress.
2018-04-11 | GSE110831 | GEO