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.
Project description:After the attachment of the lytic phage T4 to Escherichia coli cells, 1% E. coli cells showed an approximately 40-fold increase in mutant frequency. They were designated as mutator A global transcriptome analysis using microarrays was conducted to determine the difference between parental strain and mutators, and the host responce after adsorption of the phage and the ghost.
Project description:The purpose of this study is to determine whether the presence of pathogenic Escherichia coli in colon is associated with psychiatric disorders.
Project description:Despite the characterization of many aetiologic genetic changes. The specific causative factors in the development of sporadic colorectal cancer remain unclear. This study was performed to detect the possible role of Enteropathogenic Escherichia coli (EPEC) in developing colorectal carcinoma.
Project description:Purpose: In this study, Escherichia coli DH5alpha whole transcriptome sequencing was performed in order to compare the different gene expression profiles between control and exposed to Wi-Fi radiofrequency radiations. Methods:Escherichia coli DH5alpha were exposed to Wi-Fi radiations. Total RNA samples( control and exposed ) were extracted by bacteria protect-Rneasy kit,treated with DNAase and subjected to sequnecing using an Illumina-NovaSeq 6000 platform. Library preparation and sequencing were performed by Macrogen (south korea).Trimmed reads are mapped to reference genome with Bowtie. HTseq was used for expression profiling. Expression profile was calculated for each sample and gene as read count.
Project description:The Escherichia coli strain Nissle 1917 (EcN) is used as a probiotic for the treatment of certain gastrointestinal diseases in several European and non-European countries. In vitro studies showed EcN to efficiently inhibit the production of Shiga toxin (Stx) by Stx producing E. coli (STEC) such as Enterohemorrhagic E. coli (EHEC). The occurrence of the latest EHEC serotype (O104:H4) responsible for the great outbreak in 2011 in Germany was due to the infection of an enteroaggregative E. coli by a Stx 2-encoding lambdoid phage turning this E. coli into a lysogenic and subsequently into a Stx producing strain. Since EHEC infected persons are not recommended to be treated with antibiotics, EcN might be an alternative medication. However, because a harmless E. coli strain might be converted into a Stx-producer after becoming host to a stx encoding prophage, we tested EcN for stx-phage genome integration. Our experiments revealed the resistance of EcN towards not only stx-phages but also against the lambda phage. This resistance was not based on the lack of or by mutated phage receptors. Rather the expression of certain genes (superinfection exclusion B (sieB) and a phage repressor (pr) gene) of a defective prophage of EcN was involved in the complete resistance of EcN to infection by the stx- and lambda phage. Obviously, EcN cannot be turned into a Stx producer. Furthermore, we observed EcN to inactivate phages and thereby to protect E. coli K-12 strains against infection by stx- as well as lambda-phages. Inactivation of lambda-phages was due to binding of lambda-phages to LamB of EcN whereas inactivation of stx-phages was caused by a thermostable protein of EcN. These properties together with its ability to inhibit Stx production make EcN a good candidate for the prevention of illness caused by EHEC and probably for the treatment of already infected people.
Project description:Escherichia coli (E. coli) amine oxidase (ECAO) encoded by tynA gene has been one of the model enzymes to study the mechanism of oxidative deamination of amines to the corresponding aldehydes by amine oxidases. The biological roles of ECAO have been less addressed. Therefore we have constructed a gene deletion Escherichia coli K-12 strain, E. coli tynA-, and used the microarray technique to address its function by comparing the total RNA gene expression to the one of the wt. Our results suggest that tynA is a reserve gene for stringent environmental conditions and its gene product ECAO a growth advantage compared to other bacteria due to H2O2 production.
Project description:ChIP-seq was performed to map the association of FLAG-tagged CRP across the Escherichia coli MG1655 chromosome during exponential phase growth in LB alone or LB supplemented with cAMP or arabinose and IPTG. ChIP-seq was also performed to map the association of CRP across the Escherichia coli MG1655 chromosome using a CRP antibody during exponential phase growth in LB alone.
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.