Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA98043 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Genetically programmed deaths play important roles in the biology of unicellular prokaryotic cells. Some gene complexes force their maintenance on the host bacterial cells by killing cells that have lost them. This form of programmed death called post-segregational killing or genetic addiction is brought about by several Type II restriction-modification gene complexes, through restriction attack on the undermethylated chromosome, and underlie their behavior as selfish mobile elements. To learn the genetic steps to death, we examined how carriage and loss of PaeR7I restriction-modification gene complex affect host Escherichia coli cells through transcriptome and experimental analyses. The PaeR7I complex was on a temperature-sensitive plasmid so that the killing was induced by a temperature shift. We used microarrays to detail the global program of gene expression underlying cell death process mediated by PaeR7I restriction-modification system in E. coli. Keywords: time course
2009-06-23 | GSE7326 | GEO
Project description:Genetically programmed deaths play important roles in the biology of unicellular prokaryotic cells. Some gene complexes force their maintenance on the host bacterial cells by killing cells that have lost them. This form of programmed death called post-segregational killing or genetic addiction is brought about by several Type II restriction-modification gene complexes, through restriction attack on the undermethylated chromosome, and underlie their behavior as selfish mobile elements. To learn the genetic steps to death, we examined how carriage and loss of PaeR7I restriction-modification gene complex affect host Escherichia coli cells through transcriptome and experimental analyses. The PaeR7I complex was on a temperature-sensitive plasmid so that the killing was induced by a temperature shift. We used microarrays to detail the global program of gene expression underlying cell death process mediated by PaeR7I restriction-modification system in E. coli. Experiment Overall Design: Post-segregational cell killing was induced by blocking replication of a temperature sensitive plasmid carrying PaeR7I RM gene complex by shifting up the cultivation temperature. At 30℃, the permissive temperature for the plasmid replication, growth as monitored by OD660, of MG1655/pTN9 (r+m+) was indistinguishable from those of MG1655/pTN11 (r-m+) and MG1655/pHSG415 (vector). Cell death was observed at least 4 h after the temperature shift only in MG1655/pTN9 (r+m+) as in the previous works; the increase in viable cell counts stopped and resulted in decrease of cell viability. To analyze global gene expression when cells went to death, we performed transcriptome analysis 0 h, 1h, 1 h 50 min, and 3h after the temperature shift. We used Affimetrix E. coli antisense genome array. Experiments were performed independently twice.
2009-07-04 | E-GEOD-7326 | biostudies-arrayexpress
Project description:These E. coli strains were grown with various signaling molecules and the expression profiles were determined. Keywords: addition of quorum and host hormone signals
2007-09-20 | GSE7439 | GEO
Project description:PhoP is considered a regulator of virulence despite being conserved in both pathogenic and non-pathogenic Enterobacteriaceae. While Escherichia coli strains represent both non-pathogenic commensal isolates and numerous virulent pathotypes, the PhoP virulence regulator has only been studied in commensal E. coli. To better understand how conserved transcription factors contribute to virulence, we characterized PhoP in pathogenic E. coli. Loss of phoP significantly attenuated E. coli during extraintestinal infection. This was not surprising since we demonstrated that PhoP differentially regulated the transcription of >600 genes. In addition to survival at acidic pH and resistance to polymyxin B, PhoP was required for repression of motility and oxygen-independent changes in the expression of primary dehydrogenase and terminal reductase respiratory chain components. All phenotypes have in common a reliance on an energized membrane. Thus, we hypothesized that PhoP mediated these effects by regulating genes that generate a proton motive force. Indeed, bacteria lacking PhoP exhibited a hyper-polarized membrane, and dissipation of the transmembrane electrochemical gradient increased the susceptibility of the phoP mutant to acidic pH, while inhibiting respiratory generation of the proton gradient restored resistance to antimicrobial peptides independent of lipopolysaccharide modification. These findings demonstrate a connection between PhoP, virulence, and the energized state of the membrane.
2011-07-29 | GSE31029 | GEO
Project description:The purpose of this study is to determine whether the presence of pathogenic Escherichia coli in colon is associated with psychiatric disorders.
| 2230352 | ecrin-mdr-crc
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.
| 2184564 | ecrin-mdr-crc
Project description:Testing the impact of Type I Restriction Modification Systems on Gene Expression in Uropathogenic Escherichia coli
| PRJNA675406 | ENA
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
2007-12-06 | GSE9755 | GEO
Project description:PhoP is considered a regulator of virulence despite being conserved in both pathogenic and non-pathogenic Enterobacteriaceae. While Escherichia coli strains represent both non-pathogenic commensal isolates and numerous virulent pathotypes, the PhoP virulence regulator has only been studied in commensal E. coli. To better understand how conserved transcription factors contribute to virulence, we characterized PhoP in pathogenic E. coli. Loss of phoP significantly attenuated E. coli during extraintestinal infection. This was not surprising since we demonstrated that PhoP differentially regulated the transcription of >600 genes. In addition to survival at acidic pH and resistance to polymyxin B, PhoP was required for repression of motility and oxygen-independent changes in the expression of primary dehydrogenase and terminal reductase respiratory chain components. All phenotypes have in common a reliance on an energized membrane. Thus, we hypothesized that PhoP mediated these effects by regulating genes that generate a proton motive force. Indeed, bacteria lacking PhoP exhibited a hyper-polarized membrane, and dissipation of the transmembrane electrochemical gradient increased the susceptibility of the phoP mutant to acidic pH, while inhibiting respiratory generation of the proton gradient restored resistance to antimicrobial peptides independent of lipopolysaccharide modification. These findings demonstrate a connection between PhoP, virulence, and the energized state of the membrane. Comparison of gene expression between wild-type CFT073 and a CFT073 phoP deletion mutant during logarithmic phase growth in LB medium. Three biological replicates were compared from each strain.
2011-07-28 | E-GEOD-31029 | biostudies-arrayexpress
Project description:RNA-seq analysis of cells with pulsed overexpression of SdsR Most small noncoding RNAs (sRNAs) are known to base pair with target mRNAs and regulate their stability or translation with the help of Hfq to trigger various changes in cell metabolism. SdsR (also known as RyeB), which is a member of the RpoS regulon, was reported as an abundant sRNA that represses tolC and mutS in E. coli. It is known to be specific to the stationary phase and is not expressed during the exponential phase, but no previous study had examined the importance of this growth phase-dependent regulation for cell growth and survival. In this study, we examined how forced expression of SdsR during the exponential phase alters cell growth and survival. We found that ectopic expression of SdsR during the exponential phase triggered a significant and Hfq-dependent cell death. This SdsR-driven cell death was alleviated by overexpression of RyeA, an sRNA transcribed on the opposite DNA strand, suggesting that SdsR/RyeA may represent a novel type of toxin/antitoxin (T/A) system in which both the toxin and the antitoxin are sRNAs. To identify target genes involved in the observed SdsR-driven cell death, we first performed RNA-seq analysis and used the RNA-seq data to predict which SdsR-targeted mRNAs could contribute to SdsR-driven cell death. We then examined whether repression of translation of each predicted target mRNA could cause the observed SdsR-driven growth defects, and found that the SdsR-driven cell death seen in our system was mainly caused by the SdsR-mediated repression of yhcB, which encodes an inner membrane protein.
2018-12-26 | GSE116435 | GEO