EcoWG1
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB35422 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Escherichia coli is the leading cause of catheter-associated urinary tract infections, caused by biofilm formation on implanted biomaterial surfaces. Understanding the genes that cause cellular adhesion to diverse biomaterial surfaces may aid in the design of targeting anti-biofouling chemicals to prevent these biofilm infections, but our current knowledge on such surfaces is limited. Here, we incorporate a platform of six biomaterials of varying hydrophilicities and stiffnesses and a comprehensive genome-wide CRISPR interference (CRISPRi) library to elucidate genotype-phenotype relationships for cellular adhesion to physicochemically varied biomaterial surfaces in E. coli MG1655. After characterization of the biomaterials and CRISPRi tool, we designed a CRISPRi library of 34,315 unique designs targeting 99.0% of the genome in MG1655 (up to 8 designs per gene). We then performed pooled selections for adhesion to each biomaterial surface, elucidating over 400 novel gene hits to each biomaterial surface. Data analysis revealed greater correlations between biomaterials of the same hydrophilicity rather than stiffness, in addition to more gene hits associated with decreased adhesion across all six surfaces than increased adhesion. Monoclonal verification of select designs from the library exhibited strong correlations between results from the pooled selections and individual measurements for adhesion to each gel for most designs. The results from this study provide comprehensive gene sets for cellular adhesion to physicochemically diverse biomaterial surfaces that may be potential gene targets for the design of targeting anti-biofouling agents and offer insight that could be used for the design of “smart” biomaterials, both with potential to prevent biofilm infections.
2024-12-31 | GSE274727 | GEO
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:In this study, we developed a workflow to systematically and selectively induce increases in metabolites by knocking down enzymes with CRISPR interference (CRISPRi). Therefore, we created a sorted CRISPRi library targeting all 1,515 metabolic genes in the most recent genome-scale metabolic model of E. coli (iML151515). In a first step, we screened the metabolome of the CRISPRi library with a fast flow-injection mass spectrometry, which revealed strong and specific accumulation of 36% of the predicted metabolites in the iML1515 model. The accumulating metabolites were unique to certain knockdowns, especially those metabolites associated with the CRISPRi targeted-pathway.
2024-08-07 | MSV000095534 | MassIVE
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