Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA807096 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional recording Escherichia coli strain assemblies
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Project description:Transcriptional recording by CRISPR spacer acquisition from RNA
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Project description:Record-seq: Recording transcriptional histories using FsRT-Cas1–Cas2
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Project description:Recording mobile DNA in the gut microbiota using an Escherichia coli CRISPR-Cas spacer acquisition platform
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Project description:RNA-seq was performed to interogate the transcriptional changes in response to infection with Adherent Invasive E. coli and a control, non-invasive E. coli
2020-07-10 | GSE154122 | GEO
Project description:RNA-seq was performed to interogate the transcriptional changes in response to infection with Adherent Invasive E. coli and a control, non-invasive E. coli
2020-07-10 | GSE154121 | GEO
Project description:Uropathogenic Escherichia coli utilize a variety of adherence factors that assist in colonization of the host urinary tract. TosA (type one secretion) is a non-fimbrial adhesin that is predominately expressed during murine urinary tract infection (UTI), binds to kidney epithelial cells, and promotes survival during invasive infections. The tosRCBDAEF operon encodes the secretory machinery necessary for TosA localization to the E. coli cell surface, as well as the transcriptional regulator TosR. TosR binds upstream of the tos operon and, in a concentration dependent manner, either induces or represses tosA expression. TosR is a member of the PapB family of fimbrial regulators that can participate in crosstalk between fimbrial operons. TosR also binds upstream of the pap operon and suppresses PapA production. However, the scope of TosR-mediated crosstalk is understudied and may be underestimated. To quantify the global effects of TosR-mediated regulation on the E. coli CFT073 genome, we induced expression of tosR, collected mRNA, and performed RNA-Seq. These findings show that production of TosR affected the expression of genes involved with adhesins, including P, F1C, and Auf; nitrate/nitrite transport; microcin secretion; and promoted biofilm formation.
2018-04-27 | GSE112878 | GEO
Project description:The complex reservoir of metabolite-producing bacteria in the gastrointestinal tract contributes tremendously to human health and disease. Bacterial composition, and by extension gut metabolomic composition, is undoubtably influenced by the use of modern antibiotics. Herein, we demonstrate that polymyxin B, a last resort antibiotic used for chronic multidrug resistant infections infections, influences the production of the genotoxic metabolite colibactin from adherent-invasive Escherichia coli (AIEC) NC101. Colibactin can augment colorectal cancer (CRC) through DNA double stranded breaks and interstrand crosslinks. While the structure and biosynthesis of colibactin has been elucidated, chemical-induced regulation of its biosynthetic gene cluster and subsequent production of the genotoxin by pathogenic E. coli are largely unexplored. This research highlights the regulation of the colibactin-producing biosynthetic gene cluster under polymyxin stress. Using a multi-omic approach, we have identified that polymyxin stress enhances the abundance of colibactin biosynthesis proteins (Clb’s) in multiple pks+ E. coli strains, including pro-carcinogenic AIEC: NC101, the probiotic strain: E. coli Nissle 1917, and the antibiotic testing strain: E. coli ATCC 25922. Expression analysis via qPCR revealed that increased transcription of clb genes likely contributes to elevated Clb protein levels in NC101. Enhanced production of Clb’s by NC101 under polymyxin stress matched an increased production of the colibactin prodrug motif, a proxy for the mature genotoxic metabolite. Furthermore, E. coli with heightened tolerance for polymyxin antibiotics induced greater DNA damage, assessed by quantification of γH2AX staining in cultured intestinal epithelial cells. This study establishes a key link between the polymyxin B stress response and colibactin production in pks+ E. coli. Ultimately, our findings will inform future studies investigating colibactin regulation, the microbial response to antibiotics in the gut, and the ability of seemingly innocuous commensal microbes to induce host disease.
2021-07-15 | PXD025088 | Pride