Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enterobacter cloacae strain:EC-3442 | isolate:EC-3442

ABSTRACT: Enterobacter cloacae strain:EC-3442 | isolate:EC-3442 Genome sequencing and assembly

PROVIDER: PRJNA414755 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Proteomics analysis of the Enterobacter cloacae response to imipenem

Project description:Recently, we have reported on a highly drug-resistant carbapenemase-producing isolate of Enterobacter cloacae (Nepal et al., Virulence. 2018; 9: 1377-1389). In the present study, we asked the question whether and, if so, how this isolate responds to a sub-inhibitory challenge with the antibiotic imipenem. To answer this question, we applied a SILAC proteomics approach that allowed the quantification of changes in the relative abundance of bacterial protein in response to imipenem. The results show that the investigated E. cloacae isolate mounts a highly specific response to counteract the detrimental effects of imipenem.

2021-08-10 | PXD013412 | Pride

Cefazolin and Imipenem Enhance AmpC Expression and Resistance in NagZ-dependent manner in Enterobacter cloacae complex

Project description:Background: Enterobacter cloacae complex (ECC) is a common opportunistic pathogen and is responsible for causing various infections in humans. Owing to its inducible chromosomal AmpC β-lactamase (AmpC), ECC is inherently resistant to the 1st- and 2nd- generation cephalosporins. However, whether β-lactams antibiotics enhance ECC resistance remains unclear. Results: In this study, we found that subinhibitory concentrations (SICs) of cefazolin (CFZ) and imipenem (IMP) can advance the expression of AmpC and enhance its resistance towards β-lactams through NagZ in Enterobacter cloacae (EC). Further, AmpC manifested a substantial upregulation in EC in response to SICs of CFZ and IMP. In nagZ knockout EC (ΔnagZ), the resistance to β-lactam antibiotics was rather weakened and the effect of CFZ and IMP on AmpC induction was completely abrogated. NagZ ectopic expression can rescue the induction effects of CFZ and IMP on AmpC and increase ΔnagZ resistance. More importantly, CFZ and IMP have the potential to induce the expression of AmpR's target genes in a NagZ-dependent manner. Conclusions: Our findings suggest that NagZ is a critical determinant for CFZ and IMP to promote AmpC expression and resistance and that CFZ and IMP should be used with caution since they may aggravate ECC resistance. At the same time, this study further improves our understanding of resistance mechanisms in ECC.

2022-07-01 | GSE207144 | GEO

Aminoglycoside heteroresistance in Enterobacter cloacae is driven by the cell envelope stress response.

Project description:Enterobacter cloacae is a Gram-negative nosocomial pathogen of the ESKAPE priority group with increasing multi-drug resistance via the acquisition of resistance plasmids. However, E. cloacae can also display phenotypic antimicrobial resistance, such as heteroresistance or persistence. Here we report that E. cloacae ATCC 13047 and six strains isolated from patients with blood infections display heteroresistance or persistence to aminoglycosides. E. cloacae heteroresistance is transient, accompanied with formation of "petite" colonies and increased MIC against gentamicin and other aminoglycosides used in the clinic, but not other antibiotic classes. To explore the underlying mechanisms, we performed RNA sequencing of heteroresistant bacteria, which revealed global gene-expression changes and a signature of the CpxRA cell envelope stress response. Deletion of the cpxRA two-component system abrogated aminoglycoside heteroresistance and petite colony formation, pointing to its indispensable role in phenotypic resistance. The introduction of a constitutively active allele of cpxA led to high aminoglycoside MICs, consistent with cell envelope stress driving these behaviours in E. cloacae. Cell envelope stress can be caused by environmental cues, including heavy metals. Indeed, bacterial exposure to copper increased gentamicin MIC in the wild type, but not the ΔcpxRA mutant. Moreover, copper exposure also elevated the gentamicin MICs of bloodstream isolates, suggesting that CpxRA- and copper-dependent aminoglycoside resistance is broadly conserved in E. cloacae strains. Altogether, we establish that E. cloacae relies on transcriptional reprogramming via the envelope stress response pathway for transient resistance to a major class of frontline antibiotic.

2023-10-18 | GSE236124 | GEO

Enterobacter mori isolate:enterobacter cloacae

Project description:Enterobacter mori isolate:enterobacter cloacae Genome sequencing

| PRJNA663366 | ENA

Enterobacter roggenkampii isolate:enterobacter cloacae

Project description:Enterobacter roggenkampii isolate:enterobacter cloacae Genome sequencing

| PRJNA659403 | ENA

Enterobacter roggenkampii isolate:enterobacter cloacae

Project description:Enterobacter roggenkampii isolate:enterobacter cloacae Genome sequencing

| PRJNA659404 | ENA

Enterobacter mori isolate:enterobacter cloacae complex

Project description:Enterobacter mori isolate:enterobacter cloacae complex Genome sequencing

| PRJNA663254 | ENA

Enterobacter cloacae strain:NH77 | isolate:NH77

Project description:Enterobacter cloacae strain:NH77 | isolate:NH77 Genome sequencing

| PRJNA544891 | ENA

Enterobacter cloacae strain:RL8 | isolate:RL8

Project description:Enterobacter cloacae strain:RL8 | isolate:RL8 Genome sequencing

| PRJNA432310 | ENA

Enterobacter cloacae strain:CEc75 | isolate:CEc75

Project description:Enterobacter cloacae strain:CEc75 | isolate:CEc75 Genome sequencing

| PRJNA854588 | ENA

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data