EcoWG1
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB35422 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mapping the occupancy of ArcA throughout the genome of Escherchia coli MG1655 K-12 using an affinity purified antibody under anaerobic and aerobic growth conditions. As a control, we also performed ChIP-chip onArcA in a ∆arcA mutant strain of Escherchia coli MG1655 K-12. Described in the manuscript The response regulator ArcA uses a diverse binding site architechture to globally regulate carbon oxidation in E. coli
2013-10-17 | GSE46413 | GEO
Project description:Effect of sub-MIC tobramycin treatment on E. coli MG1655 WT (strain classically used as WT strain) and NCM3416 (corrected rph strain). Comparison of genes expression without treatment (MH) in E. coli MG1655 WT and NCM3416.
2023-03-01 | GSE224240 | GEO
Project description:Here, we investigated the impact of Stx2 phage carriage on Escherichia coli (E. coli) K-12 MG1655 host gene expression. Using quantitative RNA-seq analysis, we compared the transcriptome of naïve MG1655 and the lysogens carrying the Stx2 phage of the 2011 E. coli O104:H4 outbreak strain or of the E. coli O157:H7 strain PA8, which share high degree of sequence similarity.
2019-06-17 | GSE126710 | GEO
Project description:Transcriptome profiling of E. coli MG1655, E. coli EDL933, E. coli ECOR26, and E. coli Nissle 1917 grown on mouse cecal mucus as carbon source The carbon sources that support growth of pathogenic E. coli O157:H7 in the mammalian intestine have not previously been investigated. In vivo, pathogenic E. coli EDL933 primarily grows as dispersed single cells within the mucus layer that overlies the mouse cecal epithelium. We therefore compared the pathogen and commensal E. coli MG1655 for their mode of metabolism in vitro on a mixture of the sugars known to be present in cecal mucus and found that the two strains used the thirteen sugars in a similar order and co-metabolized as many as nine sugars at a time. We conducted a systematic mutational analysis of E. coli EDL933 and E. coli MG1655 with lesions in the pathways used for catabolism of thirteen mucus-derived sugars and five other compounds for which the corresponding gene system was induced in the transcriptome of cells grown on cecal mucus. Each of 18 catabolic mutants in both genetic backgrounds was fed to streptomycin-treated mice together with the respective wildtype parent strain and their colonization was monitored in fecal plate counts. None of the mutations corresponding to the five compounds not found in mucosal polysaccharides resulted in colonization defects. Based on the mutations that caused colonization defects, we determined that both E. coli EDL933 and E. coli MG1655 used arabinose, fucose, and N-acetylglucosamine in the intestine. In addition, E. coli EDL933 used galactose, hexuronates, mannose and ribose, whereas E. coli MG1655 used gluconate and N-acetylneuraminic acid. The colonization defects of six catabolic lesions were found to be additive in E. coli EDL933, but not E. coli MG1655. The data indicate that pathogenic E. coli EDL933 uses sugars that are not used by commensal E. coli MG1655 to colonize the mouse intestine. The results suggest a strategy whereby invading pathogens gain advantage by simultaneously consuming several sugars that may be available because they are not consumed by the commensal intestinal microbiota. Keywords: growth condition: carbon source was mouse cecal mucus
2008-04-25 | GSE11254 | GEO
Project description:ChIPexo experiment was performed on E. coli K12 MG1655 with various supplements designed to activate transcriptional regulators
2019-12-17 | GSE122320 | GEO
Project description:Study of the mechanisms of RecB mutant terminus DNA loss in Escherichia coli. FX158: WT MG1655 FX35: recB- FX37: ruvAB- FX51: matP- MIC18: recB- sbcD- sbcC- MIC20: recB- ruvAB- MIC24: matP- recB- MIC25: recA- recB- MIC31: sbcB- sbcD- MIC34: recA- recD- MIC40: linear chromosome MIC41: linear chromosome recB- MIC42: matP- ftsKC- MIC43: matP- ftsKC- recB- MIC48: recA- Cells were grown in M9 minimal medium supplemented with 0.4 % glucose to exponential phase (0.2 OD 650 nm). Chromosomal DNA was extracted using the Sigma GenElute bacterial genomic DNA kit. 5 μg of DNA were used to generate a genomic library according to Illumina's protocol. The libraries and the sequencing were performed by the High-throughput Sequencing facility of the I2BC (http://www.i2bc.paris-saclay.fr/spip.php?article399&lang=en, CNRS, Gif-sur-Yvette, France). Genomic DNA libraries were made with the ‘Nextera DNA library preparation kit’ (Illumina) following the manufacturer’s recommendations. Library quality was assessed on an Agilent Bioanalyzer 2100, using an Agilent High Sensitivity DNA Kit (Agilent technologies). Libraries were pooled in equimolar proportions. 75 bp single reads were generated on an Illumina MiSeq instrument, using a MiSeq Reagent kit V2 (500 cycles) (Illumina), with an expected depth of 217X. An in-lab written MATLAB-based script was used to perform marker frequency analysis. Reads were aligned on the Escherichia coli K12 MG1655 genome using BWA software. Data were normalized by dividing uniquely mapping sequence reads by the total number of reads. Enrichment of uniquely mapping sequence reads in 1 kb non-overlapping windows were calculated and plotted against the chromosomal coordinates.
2017-11-10 | E-MTAB-6122 | biostudies-arrayexpress
Project description:The gene expression profile of E. coli K-12 MG1655 grown in minimal medium treated with 0.12 mg/L of the biocide triclosan has been analysed using whole genome oligonucleotide microarrays. "Control" RNA was isolated from three independently grown 50ml MOPS minimal media cultures of E. coli K-12 MG1655. “Test” RNA was isolated from three independently grown 50ml MOPS minimal cultures of E. coli K-12 MG1655, to which was added 0.12 mg/L of triclosan after reaching mid-logarithmic growth phase (OD600 ~ 0.7 +/- 0.02). Keywords: dose response
2009-08-20 | GSE15059 | GEO
Project description:Escherichia coli O157 presents a number of specific problems in terms of food safety and public health. It has been found that E. coli O157 is more resistant to a number of the stresses encountered during food production such as heat, pH and osmotic shock. This greater resistance is thought to contribute to the low infectious dose of E. coli O157 (<100 organisms). Moreover, E. coli O157 is associated with debilitating conditions such as haemorrhagic colitis and haemoytic uraemic syndrome, particularly in children and the elderly. We have been studying the stress responses of E. coli O157:H7 (Sakai) and comparing with a commensal strain of E. coli K-12, MG1655. We found that E. coli O157 (Sakai) is more sensitive to oxidative stress than MG1655. A microarray study of these strains treated with sub-lethal concentrations (0.5mg/ml) of menadione revealed big differences in their responses. In E. coli O157 (Sakai), 540 genes responded significantly to the treatment compared to 121 genes in MG1655. One surprising finding from the microarray data was the observation that many iron-transport genes were up-regulated in E. coli O157 (Sakai) whereas relatively few were induced in MG1655 despite the fact that the bacteria were grown in a medium containing ample iron. We speculated that the induction of iron transport genes in an iron-rich medium might have contributed to the enhanced killing of E. coli O157 (Sakai) through triggering of a Fenton reaction. We speculated that the difference in sensitivity to oxidative stress might be due to differences in the intracellular iron content of E. coli O157 and MG1655. We found that E. coli O157 contains ~50% more iron than MG1655 and believe that during oxidative stress, this iron is released by damaged proteins. The greater levels of free iron in E. coli O157 will trigger a greater Fenton reaction that can damage the ferric uptake regulator (Fur), resulting in unregulated iron transport. In MG1655, the lower iron content results in a smaller Fenton reaction, enabling the cellular protection systems to limit damage and protect Fur.
2015-02-22 | GSE36130 | GEO