Escherichia coli
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ABSTRACT:
PROVIDER: PRJNA689933 | ENA |
REPOSITORIES: ENA
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Project description:The strategy of a novel way to enhance bacterial motility
| PRJNA693394 | ENA
Project description:Many neutralophilic bacterial species try to evade acid stress with an escape strategy, which is reflected in the increased expression of genes coding for flagellar components. Extremely acid-tolerant bacteria, such as Escherichia coli, survive the strong acid stress, e.g. in the stomach of vertebrates. Recently, we were able to show that the induction of motility genes in E. coli is strictly dependent on the degree of acid stress, i.e. they are induced under mild acid stress but not under severe acid stress. However, it was not known to what extent fine-tuned expression of motility genes is related to fitness and the ability to survive periods of acid shock. In this study, we demonstrate that the expression of FlhDC, the master regulator of flagellation, is inversely correlated with acid shock survival of E. coli. We encountered this phenomenon when analyzing mutants from the Keio collection in which the expression of flhDC was altered by an IS element. These results suggest a fitness trade-off between acid tolerance and motility.
2024-04-14 | GSE260455 | GEO
Project description:Antibiotic resistance is increasingly becoming a serious challenge to public health. The regulation of metabolism by post-translational modifications (PTMs) has been widely studied; however, the comprehensive mechanism underlying the regulation of acetylation in bacterial resistance against antibiotics is unknown. Herein, with Escherichia coli as the model, we performed quantitative analysis of the acetylated proteome of wild-type sensitive strain (WT) and ampicillin- (Re-Amp), kanamycin- (Re-Kan), and polymyxin B-resistant (Re-Pol) strains. Based on bioinformatics analysis combined with biochemical validations, we found that a common regulatory mechanism exists between the different resistant strains. Acetylation negatively regulates bacterial metabolism to maintain antibiotic resistance, but positively regulates bacterial motility. Further analyses revealed that key enzymes in various metabolic pathways were differentially acetylated. Particularly, pyruvate kinase (PykF), a key glycolytic enzyme regulating bacterial metabolism, and its acetylated form were highly expressed in the three resistant types and were identified as reversibly acetylated by the deacetylase CobB and the acetyl-transferase PatZ, and also could be acetylated by non-enzyme AcP in vitro. Further, the deacetylation of Lys413 of PykF increased the enzyme activity by changing the conformation of ATP binding site of PykF, resulting in an increase in energy production, which in turn increased the sensitivity of drug-resistant strains to antibiotics. This study provides novel insights for understanding bacterial resistance and lays the foundation for future research on regulation of acetylation in antibiotic-resistant strains.
2022-10-14 | PXD030283 | Pride
Project description:Background: Antibiotic resistance is an urgent threat to public health. Prior to the evolution of antibiotic resistance, bacteria frequently undergo response and tend to develop a state of adaption to the antibiotic. Ciprofloxacin is a broad-spectrum antibiotic by damaging DNA. With the widespread clinical application, the resistance of bacteria to ciprofloxacin continues to increase. This study aimed to investigate the transcriptome changes under the action of high concentration of ciprofloxacin in Escherichia coli. Results: We identified 773 up-regulated differentially expressed genes (DEGs) and 645 down-regulated DEGs in ciprofloxacin treated cells. Enriched biological pathways reflected the up-regulation of biological process such as DNA damage and repair system, toxin/antitoxin systems, formaldehyde detoxification system, peptide biosynthetic process and cellular protein metabolic process. With KEGG pathway analysis, up-regulated DEGs of kdsA and waa operon were associated with “LPS biosynthesis”. rfbABC operon was related to “streptomycin biosynthesis” and “polyketide sugar unit biosynthesis ”. Down-regulated DEGs of thrABC and fliL operons were associated with “flagellum-dependent cell motility” and “bacterial-type flagellum” in GO terms, and enriched into “biosynthesis of amino acids” and “flagellar assembly” in KEGG pathways. After treatment of ciprofloxacin, bacterial lipopolysacchride (LPS) release was increased by two times, and the mRNA expression level of LPS synthesis genes, waaB, waaP and waaG were elevated (P < 0.05). Conclusions: Characterization of the gene clusters by RNA-seq showed high dose of ciprofloxacin not only lead to damage of bacterial macromolecules and components, but also induce protective response against antibiotic action by up-regulating the SOS system, toxin/antitoxin system and formaldehyde detoxification system. Moreover, genes related to biosynthesis of LPS were also upregulated by the treatment indicating that ciprofloxacin can enhance the production of endotoxin on the level of transcription. These results demonstrated that transient exposure of high dose ciprofloxacin is double edged. Cautions should be taken when administering the high dose antibiotic treatment for infectious diseases.
2020-06-16 | GSE152445 | GEO
Project description:Specific recognition and bacterial adhesion to host cells by uropathogenic E. coli (UPEC) are the first steps towards infection of epithelial tissue of the human urogenital system. Therefore, targeting of UPEC virulence factors, relevant for adhesion, is a promising approach for prevention of recurrent urinary tract infections (UTI). A fully characterized plant-derived aqueous extract from the leaves of Orthosiphon stamineus (OWE), a plant traditionally used in clinical practice in Europe and Asia for UTI, has been shown to exert strong antiadhesive effects under in vitro and in vivo conditions. For improved understanding of the underlying mechanisms transcriptome analysis of OWE-treated UPEC strain UTI89 by Illumina sequencing and cross-validation of these data by qPCR indicated significant down-regulation of bacterial adhesins (curli, type 1-, F1C- and P fimbriae) and of the chaperone-mediated protein folding/unfolding and pilus assembly process; in contrast flagellar and motility-related genes were upregulated. We conclude that OWE transforms the sessile lifestyle of bacteria into a motile one and therefore disables bacterial attachment to the host cell. Additionally, the extract inhibited gene expression of multiple iron acquisition systems (Ent, Fep, Feo, Fhu, Chu, Sit, Ybt) concomitant with an upregulated expression of the ferric uptake regulator (Fur) repressor. The present study explains the antiadhesive and antiinfective effect of the plant extract by pinpointing specific biochemical and molecular targets.
2019-05-18 | GSE131382 | GEO
Project description:Human Peptidoglycan Recognition Proteins (PGRPs) kill bacteria, likely by over-activating stress responses in bacteria. To gain insight into the mechanism of PGRP killing of Escherichia coli and bacterial defense against PGRP killing, gene expression in E. coli treated with a control protein (bovine serum albumin, BSA), human recombinant PGRP (PGLYRP4), gentamicin (aminoglycoside antibiotic), and CCCP (membrane potential decoupler) were compared. Each treatment induced unique and somewhat overlapping pattern of gene expression. PGRP highly increased expression of genes for oxidative and disulfide stress, detoxification and efflux of Cu, As, and Zn, repair of damaged proteins and DNA, methionine and histidine synthesis, energy generation, and Fe-S clusters repair. PGRP also caused marked decrease in the expression of genes for Fe uptake and motility. Gene expression microarray in E. coli exposed to a human bactericidal innate immunity protein, PGRP, showed induction of oxidative stress response and defense genes, with different expression pattern than E. coli exposed to an aminoglycoside antibiotic and a membrane potential decoupler.
2014-07-25 | GSE44211 | GEO
Project description:Bacterial metabolites are substrates of virulence factors of uropathogenic Escherichia coli (UPEC), but the mechanism underlying the role of functional metabolites in bacterial virulence from the perspective of small molecular metabolism is unclear. In the present study, we used a strategy of functional metabolomics integrated with bacterial genetics in attempt to decipher the mechanism of virulence formation in Escherichia coli (E. coli) from the viewpoint of small molecule metabolism. We identified the virulence-associated metabolome via analysis of the primary metabolome of the pathogenic UTI89 strain and the non-pathogenic MG1655 strain. Then, the iron-mediated virulence associated metabolome was identified by an iron fishing strategy. Also, the mechanism of siderophores in regulating pathogenicity in different environments was explored by investigating the effect of iron on siderophore biosynthesis. Finally, by knocking out genes related to siderophore biosynthesis, siderophore transport and iron utilization, siderophores dependent iron-regulating virulence associated metabolome, including 18 functional metabolites, was identified and verified to be involved in the regulation of bacterial virulence. Based on this we found that these functional metabolites regulated the virulence of E. coli by targeting multiple metabolic pathways in an iron-siderophores dependent manner. Moreover, a quantitative proteomics approach was implemented to further elucidate the mechanism of functional metabolites and functional proteins in modulating bacterial virulence. And our findings demonstrated that functional proteins regulated the virulence of E. coli by mediating iron binding, iron-siderophore transmembrane transport, and the biosynthesis and expression of functional metabolites. Interestingly, we found that functional metabolites enhance the virulence of E. coli by specifically modulating the key metabolic pathways involved in purine metabolism, proline metabolism, arginine metabolism and pyrimidine metabolism. Taken together, our study identified for the first time 18 functional metabolites regulating the of E. coli virulence, greatly enriching our understanding of the mechanism of functional metabolites that regulate the E. coli virulence by targeting primary metabolism, which will largely contribute to the development of new strategies to target virulence-based diagnosis and therapy of infections caused by different pathogens.
2022-03-25 | ST002131 | MetabolomicsWorkbench
Project description:Bacterial metabolites are substrates of virulence factors of uropathogenic Escherichia coli (UPEC), but the mechanism underlying the role of functional metabolites in bacterial virulence from the perspective of small molecular metabolism is unclear. In the present study, we used a strategy of functional metabolomics integrated with bacterial genetics in attempt to decipher the mechanism of virulence formation in Escherichia coli (E. coli) from the viewpoint of small molecule metabolism. We identified the virulence-associated metabolome via analysis of the primary metabolome of the pathogenic UTI89 strain and the non-pathogenic MG1655 strain. Then, the iron-mediated virulence associated metabolome was identified by an iron fishing strategy. Also, the mechanism of siderophores in regulating pathogenicity in different environments was explored by investigating the effect of iron on siderophore biosynthesis. Finally, by knocking out genes related to siderophore biosynthesis, siderophore transport and iron utilization, siderophores dependent iron-regulating virulence associated metabolome, including 18 functional metabolites, was identified and verified to be involved in the regulation of bacterial virulence. Based on this we found that these functional metabolites regulated the virulence of E. coli by targeting multiple metabolic pathways in an iron-siderophores dependent manner. Moreover, a quantitative proteomics approach was implemented to further elucidate the mechanism of functional metabolites and functional proteins in modulating bacterial virulence. And our findings demonstrated that functional proteins regulated the virulence of E. coli by mediating iron binding, iron-siderophore transmembrane transport, and the biosynthesis and expression of functional metabolites. Interestingly, we found that functional metabolites enhance the virulence of E. coli by specifically modulating the key metabolic pathways involved in purine metabolism, proline metabolism, arginine metabolism and pyrimidine metabolism. Taken together, our study identified for the first time 18 functional metabolites regulating the of E. coli virulence, greatly enriching our understanding of the mechanism of functional metabolites that regulate the E. coli virulence by targeting primary metabolism, which will largely contribute to the development of new strategies to target virulence-based diagnosis and therapy of infections caused by different pathogens.
2022-03-23 | ST002128 | MetabolomicsWorkbench
Project description:Bacterial metabolites are substrates of virulence factors of uropathogenic Escherichia coli (UPEC), but the mechanism underlying the role of functional metabolites in bacterial virulence from the perspective of small molecular metabolism is unclear. In the present study, we used a strategy of functional metabolomics integrated with bacterial genetics in attempt to decipher the mechanism of virulence formation in Escherichia coli (E. coli) from the viewpoint of small molecule metabolism. We identified the virulence-associated metabolome via analysis of the primary metabolome of the pathogenic UTI89 strain and the non-pathogenic MG1655 strain. Then, the iron-mediated virulence associated metabolome was identified by an iron fishing strategy. Also, the mechanism of siderophores in regulating pathogenicity in different environments was explored by investigating the effect of iron on siderophore biosynthesis. Finally, by knocking out genes related to siderophore biosynthesis, siderophore transport and iron utilization, siderophores dependent iron-regulating virulence associated metabolome, including 18 functional metabolites, was identified and verified to be involved in the regulation of bacterial virulence. Based on this we found that these functional metabolites regulated the virulence of E. coli by targeting multiple metabolic pathways in an iron-siderophores dependent manner. Moreover, a quantitative proteomics approach was implemented to further elucidate the mechanism of functional metabolites and functional proteins in modulating bacterial virulence. And our findings demonstrated that functional proteins regulated the virulence of E. coli by mediating iron binding, iron-siderophore transmembrane transport, and the biosynthesis and expression of functional metabolites. Interestingly, we found that functional metabolites enhance the virulence of E. coli by specifically modulating the key metabolic pathways involved in purine metabolism, proline metabolism, arginine metabolism and pyrimidine metabolism. Taken together, our study identified for the first time 18 functional metabolites regulating the of E. coli virulence, greatly enriching our understanding of the mechanism of functional metabolites that regulate the E. coli virulence by targeting primary metabolism, which will largely contribute to the development of new strategies to target virulence-based diagnosis and therapy of infections caused by different pathogens.
2022-03-25 | ST002129 | MetabolomicsWorkbench
Project description:Bacterial metabolites are substrates of virulence factors of uropathogenic Escherichia coli (UPEC), but the mechanism underlying the role of functional metabolites in bacterial virulence from the perspective of small molecular metabolism is unclear. In the present study, we used a strategy of functional metabolomics integrated with bacterial genetics in attempt to decipher the mechanism of virulence formation in Escherichia coli (E. coli) from the viewpoint of small molecule metabolism. We identified the virulence-associated metabolome via analysis of the primary metabolome of the pathogenic UTI89 strain and the non-pathogenic MG1655 strain. Then, the iron-mediated virulence associated metabolome was identified by an iron fishing strategy. Also, the mechanism of siderophores in regulating pathogenicity in different environments was explored by investigating the effect of iron on siderophore biosynthesis. Finally, by knocking out genes related to siderophore biosynthesis, siderophore transport and iron utilization, siderophores dependent iron-regulating virulence associated metabolome, including 18 functional metabolites, was identified and verified to be involved in the regulation of bacterial virulence. Based on this we found that these functional metabolites regulated the virulence of E. coli by targeting multiple metabolic pathways in an iron-siderophores dependent manner. Moreover, a quantitative proteomics approach was implemented to further elucidate the mechanism of functional metabolites and functional proteins in modulating bacterial virulence. And our findings demonstrated that functional proteins regulated the virulence of E. coli by mediating iron binding, iron-siderophore transmembrane transport, and the biosynthesis and expression of functional metabolites. Interestingly, we found that functional metabolites enhance the virulence of E. coli by specifically modulating the key metabolic pathways involved in purine metabolism, proline metabolism, arginine metabolism and pyrimidine metabolism. Taken together, our study identified for the first time 18 functional metabolites regulating the of E. coli virulence, greatly enriching our understanding of the mechanism of functional metabolites that regulate the E. coli virulence by targeting primary metabolism, which will largely contribute to the development of new strategies to target virulence-based diagnosis and therapy of infections caused by different pathogens.
2022-03-25 | ST002130 | MetabolomicsWorkbench