Faculty Opinions recommendation of A novel application of gene arrays: Escherichia coli array provides insight into the biology of the obligate endosymbiont of tsetse flies.

2001 ◽  
Author(s):  
Sara Melville
Keyword(s):  
Escherichia Coli ◽  
Tsetse Flies ◽  
Gene Arrays ◽  
Insight Into ◽  
Obligate Endosymbiont

scholarly journals Chi-Dependent Intramolecular Recombination in Escherichia coli

Genetics ◽  
1998 ◽  
Vol 148 (2) ◽  
pp. 545-557
Author(s):  
Rachel Friedman-Ohana ◽  
Iris Karunker ◽  
Amikam Cohen
Keyword(s):  
Escherichia Coli ◽  
Homologous Recombination ◽  
Experimental System ◽  
Cis Acting ◽  
Enzymes Activity ◽  
Intramolecular Recombination ◽  
Insight Into

Abstract Homologous recombination in Escherichia coli is enhanced by a cis-acting octamer sequence named Chi (5′-GCTGGTGG-3′) that interacts with RecBCD. To gain insight into the mechanism of Chi-enhanced recombination, we recruited an experimental system that permits physical monitoring of intramolecular recombination by linear substrates released by in vivo restriction from infecting chimera phage. Recombination of the released substrates depended on recA, recBCD and cis-acting Chi octamers. Recombination proficiency was lowered by a xonA mutation and by mutations that inactivated the RuvABC and RecG resolution enzymes. Activity of Chi sites was influenced by their locations and by the number of Chi octamers at each site. A single Chi site stimulated recombination, but a combination of Chi sites on the two homologs was synergistic. These data suggest a role for Chi at both ends of the linear substrate. Chi was lost in all recombinational exchanges stimulated by a single Chi site. Exchanges in substrates with Chi sites on both homologs occurred in the interval between the sites as well as in the flanking interval. These observations suggest that the generation of circular products by intramolecular recombination involves Chi-dependent processing of one end by RecBCD and pairing of the processed end with its duplex homolog.

scholarly journals Overproduction of SecA Suppresses the Export Defect Caused by a Mutation in the Gene Encoding the Escherichia coli Export Chaperone SecB

1999 ◽  
Vol 181 (10) ◽  
pp. 3010-3017 ◽  
Author(s):  
Heather A. Cook ◽  
Carol A. Kumamoto
Keyword(s):  
Escherichia Coli ◽  
Outer Membrane Proteins ◽  
Protein A ◽  
In Vivo Studies ◽  
Wild Type ◽  
Gene Encoding ◽  
Precursor Proteins ◽  
Additional Support ◽  
Insight Into

ABSTRACT SecB is a cytosolic protein required for rapid and efficient export of particular periplasmic and outer membrane proteins inEscherichia coli. SecB promotes export by stabilizing newly synthesized precursor proteins in a nonnative conformation and by targeting the precursors to the inner membrane. Biochemical studies suggest that SecB facilitates precursor targeting by binding to the SecA protein, a component of the membrane-embedded translocation apparatus. To gain more insight into the functional interaction of SecB and SecA, in vivo, mutations in the secA locus that compensate for the export defect caused by the secBmissense mutation secBL75Q were isolated. Two suppressors were isolated, both of which led to the overproduction of wild-type SecA protein. In vivo studies demonstrated that the SecBL75Q mutant protein releases precursor proteins at a lower rate than does wild-type SecB. Increasing the level of SecA protein in the cell was found to reverse this slow-release defect, indicating that overproduction of SecA stimulates the turnover of SecBL75Q-precursor complexes. These findings lend additional support to the proposed pathway for precursor targeting in which SecB promotes targeting to the translocation apparatus by binding to the SecA protein.

Interactions between adherent-invasive Escherichia coli and host macrophages: a virulence phenotype.

2021 ◽  
Author(s):  
Michael John Dill Renouf
Keyword(s):  
Escherichia Coli ◽  
Secondary Infection ◽  
Opportunistic Pathogen ◽  
Intracellular Survival ◽  
Western World ◽  
Infection Model ◽  
Raw264.7 Macrophages ◽  
Bacterial Uptake ◽  
Inflammatory Bowel ◽  
Insight Into

Inflammatory bowel disease (IBD) is a chronic condition increasing in prevalence throughout the western world and in developing countries. Adherent-invasive Escherichia coli (AIEC) are an opportunistic pathogen associated with IBD. Well-characterized genetic risk factors for IBD include mutations in genes associated with host-cell autophagy. A phenotype of interest in AIEC pathogenesis is survival within host macrophages. Intracellular survival of AIEC strains has been correlated with existing virulence factors but no single factor has been identified to explain this behaviour. In this thesis, infections of RAW264.7 macrophages with AIEC strains from diverse sources demonstrates increased frequency of both bacterial uptake and intracellular survival in disease-associated strains. A secondary infection model reveals the effect of primary AIEC infection on downstream macrophage function and a novel phenotype was identified in the disease-associated strain HM605. Co-localization using fluorescence microscopy shows changes in intracellular trafficking of HM605. This work aims to provide insight into one bacterial phenotype that contributes to the development of disease

scholarly journals Comparative genomic analysis provides insight into the phylogeny and virulence of atypical enteropathogenic Escherichia coli strains from Brazil

2020 ◽  
Vol 14 (6) ◽  
pp. e0008373 ◽  
Author(s):  
Rodrigo T. Hernandes ◽  
Tracy H. Hazen ◽  
Luís F. dos Santos ◽  
Taylor K. S. Richter ◽  
Jane M. Michalski ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Genomic Analysis ◽  
Comparative Genomic Analysis ◽  
Comparative Genomic ◽  
Enteropathogenic Escherichia Coli ◽  
Insight Into

scholarly journals Multiomics Analysis Provides Insight into the Laboratory Evolution of Escherichia coli toward the Metabolic Usage of Fluorinated Indoles

2020 ◽  
Author(s):  
Federica Agostini ◽  
Ludwig Sinn ◽  
Daniel Petras ◽  
Christian J. Schipp ◽  
Vladimir Kubyshkin ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Laboratory Evolution ◽  
Insight Into

scholarly journals Using a Chemical Genetic Screen to Enhance Our Understanding of the Antimicrobial Properties of Gallium against Escherichia coli

Genes ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 34 ◽  
Author(s):  
Natalie Gugala ◽  
Kate Chatfield-Reed ◽  
Raymond J. Turner ◽  
Gordon Chua
Keyword(s):  
Escherichia Coli ◽  
Cell Envelope ◽  
Antimicrobial Properties ◽  
Iron Sulfur Cluster ◽  
Nucleotide Biosynthesis ◽  
E Coli ◽  
Chemical Genetic ◽  
Iron Sulfur ◽  
Insight Into ◽  
Mutant Collection

The diagnostic and therapeutic agent gallium offers multiple clinical and commercial uses including the treatment of cancer and the localization of tumors, among others. Further, this metal has been proven to be an effective antimicrobial agent against a number of microbes. Despite the latter, the fundamental mechanisms of gallium action have yet to be fully identified and understood. To further the development of this antimicrobial, it is imperative that we understand the mechanisms by which gallium interacts with cells. As a result, we screened the Escherichia coli Keio mutant collection as a means of identifying the genes that are implicated in prolonged gallium toxicity or resistance and mapped their biological processes to their respective cellular system. We discovered that the deletion of genes functioning in response to oxidative stress, DNA or iron–sulfur cluster repair, and nucleotide biosynthesis were sensitive to gallium, while Ga resistance comprised of genes involved in iron/siderophore import, amino acid biosynthesis and cell envelope maintenance. Altogether, our explanations of these findings offer further insight into the mechanisms of gallium toxicity and resistance in E. coli.

scholarly journals The Influence of Repressor DNA Binding Site Architecture on Transcriptional Control

mBio ◽  
2014 ◽  
Vol 5 (5) ◽  
Author(s):  
Dan M. Park ◽  
Patricia J. Kiley
Keyword(s):  
Escherichia Coli ◽  
Dna Binding ◽  
Binding Site ◽  
Information Content ◽  
Fine Tuning ◽  
Carbon Oxidation ◽  
Content Type ◽  
Architectural Features ◽  
Recognition Elements ◽  
Insight Into

ABSTRACTHow the architecture of DNA binding sites dictates the extent of repression of promoters is not well understood. Here, we addressed the importance of the number and information content of the three direct repeats (DRs) in the binding and repression of theicdApromoter by the phosphorylated form of the globalEscherichia colirepressor ArcA (ArcA-P). We show that decreasing the information content of the two sites with the highest information (DR1 and DR2) eliminated ArcA binding to all three DRs and ArcA repression oficdA. Unexpectedly, we also found that DR3 occupancy functions principally in repression, since mutation of this low-information-content site both eliminated DNA binding to DR3 and significantly weakenedicdArepression, despite the fact that binding to DR1 and DR2 was intact. In addition, increasing the information content of any one of the three DRs or addition of a fourth DR increased ArcA-dependent repression but perturbed signal-dependent regulation of repression. Thus, our data show that the information content and number of DR elements are critical architectural features for maintaining a balance between high-affinity binding and signal-dependent regulation oficdApromoter function in response to changes in ArcA-P levels. Optimization of such architectural features may be a common strategy to either dampen or enhance the sensitivity of DNA binding among the members of the large OmpR/PhoB family of regulators as well as other transcription factors.IMPORTANCEInEscherichia coli, the response regulator ArcA maintains homeostasis of redox carriers under O2-limiting conditions through a comprehensive repression of carbon oxidation pathways that require aerobic respiration to recycle redox carriers. Although a binding site architecture comprised of a variable number of sequence recognition elements has been identified within the promoter regions of ArcA-repressed operons, it is unclear how this variable architecture dictates transcriptional regulation. By dissecting the role of multiple sequence elements within theicdApromoter, we provide insight into the design principles that allow ArcA to repress transcription within diverse promoter contexts. Our data suggest that the arrangement of recognition elements is tailored to achieve sufficient repression of a given promoter while maintaining appropriate signal-dependent regulation of repression, providing insight into how diverse binding site architectures link changes in O2with the fine-tuning of carbon oxidation pathway levels.

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