Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA433505 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6703077.fastq.gz | Fastqsanger.gz |
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Project description:Escherichia coli O157:H7 is an important food-borne pathogen that can cause hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS) in humans. pO157_Sal, a novel conjugative plasmid is present in a Chinese O157:H7 outbreak strain Xuzhou21. Here we investigated the phenotypic and transcriptional differences between the wild type strain Xuzhou21 and the pO157_Sal cured mutant strain Xuzhou21m. RNA-seq analysis found that all 52 ORFs encoded on pO157_Sal were transcribed. 168 chromosomal and pO157 genes were differentially expressed (≥2 fold difference) between Xuzhou21 and Xuzhou21m. Sixty-seven and 101 genes were up-regulated and down-regulated respectively by pO157_Sal including genes related to stress response, adaption and virulence. The plasmid-cured mutant grew slower than wild type in M9 medium under the condition of high NaCl or presence of sodium deoxycholate (NaDC), corroborating with the RNA-seq data. Seven differentially expressed genes are associated with NaDC resistance, including the adenine-specific DNA-methyltransferase gene (dam), multidrug efflux system subunit gene mdtA, hyperosmotically inducible periplasmic protein gene osmY and oxidation-reduction related genes while two differentially expressed genes (osmY and pspD) are likely to be related to resistance to osmotic pressure. A number of differentially expressed genes were virulence associated including four genes encoding T3SS effectors from the chromosome and ehxD from pO157. These findings demonstrated that the plasmid pO157_Sal affects the chromosome and pO157 genes transcription and contributes to the enhanced ability to resist stress. We conclude that pO157_Sal plays an important role in regulating global gene expression and affects virulence and adaptation of E.coli O157:H7.
2013-03-05 | GSE44846 | GEO
Project description:Escherichia coli O157:H7 is an important food-borne pathogen that can cause hemorrhagic colitis (HC) and hemolytic-uremic syndrome (HUS) in humans. pO157_Sal, a novel conjugative plasmid is present in a Chinese O157:H7 outbreak strain Xuzhou21. Here we investigated the phenotypic and transcriptional differences between the wild type strain Xuzhou21 and the pO157_Sal cured mutant strain Xuzhou21m. RNA-seq analysis found that all 52 ORFs encoded on pO157_Sal were transcribed. 168 chromosomal and pO157 genes were differentially expressed (M-bM-^IM-%2 fold difference) between Xuzhou21 and Xuzhou21m. Sixty-seven and 101 genes were up-regulated and down-regulated respectively by pO157_Sal including genes related to stress response, adaption and virulence. The plasmid-cured mutant grew slower than wild type in M9 medium under the condition of high NaCl or presence of sodium deoxycholate (NaDC), corroborating with the RNA-seq data. Seven differentially expressed genes are associated with NaDC resistance, including the adenine-specific DNA-methyltransferase gene (dam), multidrug efflux system subunit gene mdtA, hyperosmotically inducible periplasmic protein gene osmY and oxidation-reduction related genes while two differentially expressed genes (osmY and pspD) are likely to be related to resistance to osmotic pressure. A number of differentially expressed genes were virulence associated including four genes encoding T3SS effectors from the chromosome and ehxD from pO157. These findings demonstrated that the plasmid pO157_Sal affects the chromosome and pO157 genes transcription and contributes to the enhanced ability to resist stress. We conclude that pO157_Sal plays an important role in regulating global gene expression and affects virulence and adaptation of E.coli O157:H7. The total mRNA extracted from Escherichia coli O157:H7 Xuzhou21 and its plasmid cured strain Xuzhou21m were sequenced using Illumina.
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Project description:Plasmid sequencing of tetracycline resistance genes harbouring plasmid.
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Project description:Plasmid sequencing of tetracycline resistance genes harbouring plasmid.
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Project description:Plasmid sequencing of tetracycline resistance genes harbouring plasmid.
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Project description:Gene expression profiles of Escherichia coli, grown anaerobically, with or without Acacia mearnsii (Black wattle) extract were compared to identify tannin-resistance strategies. The cell envelope stress protein, spy, and the multidrug transporter-encoding mdtABCD, both under the control of the BaeSR two-component regulatory system, were significantly up-regulated in the presence of tannins. BaeSR mutants were more tannin-sensitive than their wild-type counterparts. Keywords: tannin resistance
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Project description:Host acquisition by bacteriophages (phages) often entails modulation, appropriation, or inhibition of components and processes central to bacterial gene expression. Among these, small non‑coding RNAs (sRNAs) are major regulators of RNA fate and frequently rely on the conserved RNA chaperone Hfq to engage their cognate targets. Although phages are known to encode specialised proteins and sRNAs to manipulate host gene expression, it has remained unclear whether they also co‑opt host‑encoded sRNAs for their own gene regulatory needs. We show that transcriptome‑wide Hfq‑mediated RNA–RNA interactions are broadly destabilised during T2 phage infection of Escherichia coli. We further demonstrate that the conserved bacterial sRNA ArcZ is co-opted by T2 to promote expression of a conserved phage operon that includes a protein inhibiting a bacterial restriction–modification system. ArcZ achieves this by preventing RNase E–mediated degradation of the transcript originating from the phage operon. Our study provides the first evidence of an evolutionary strategy in which a phage leverages a nucleic acid host factor to fulfil its own gene expression requirements.
2026-05-18 | GSE330885 | GEO
Project description:Host acquisition by bacteriophages (phages) often entails modulation, appropriation, or inhibition of components and processes central to bacterial gene expression. Among these, small non‑coding RNAs (sRNAs) are major regulators of RNA fate and frequently rely on the conserved RNA chaperone Hfq to engage their cognate targets. Although phages are known to encode specialised proteins and sRNAs to manipulate host gene expression, it has remained unclear whether they also co‑opt host‑encoded sRNAs for their own gene regulatory needs. We show that transcriptome‑wide Hfq‑mediated RNA–RNA interactions are broadly destabilised during T2 phage infection of Escherichia coli. We further demonstrate that the conserved bacterial sRNA ArcZ is co-opted by T2 to promote expression of a conserved phage operon that includes a protein inhibiting a bacterial restriction–modification system. ArcZ achieves this by preventing RNase E–mediated degradation of the transcript originating from the phage operon. Our study provides the first evidence of an evolutionary strategy in which a phage leverages a nucleic acid host factor to fulfil its own gene expression requirements.
2026-05-23 | GSE331271 | GEO
Project description:MgrR is a newly characterized Hfq dependent small RNA RNA. The expression of MgrR is regulated by Two component system, PhoPQ regulon, which senses low Mg2+ in environment. It has been reported that Hfq-binding sRNAs base pair with target RNAs, frequently leading to rapid degradation of target messages or, less frequently, to stabilization, both of which can be assayed by using microarrays. In order to search for the target genes of MgrR, we therefore examined the consequences of MgrR expression on mRNA abundance under two conditions. In condition 1, the chromosomal copy of mgrR was deleted and MgrR was expressed for 15’ from an induced plac-mgrR plasmid and compared to cells carrying a vector induced for the same period. In condition 2, the expression of mRNAs was compared in wild-type cells (mgrR+) and the mgrR deletion strain, both grown in LB; because MgrR levels are fairly high under our normal growth conditions, this allowed analysis of both the direct and indirect (long-term) effects of MgrR.
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