Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Enterobacter cloacae BWH 31

ABSTRACT: Enterobacter cloacae BWH 31 Genome sequencing and assembly

PROVIDER: PRJNA201971 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	AYIP01.dat.gz	Other
	AYIP01.fasta.gz	Fasta.gz
	AYIP01.master.dat	Other
	SRR850659_1.fastq.gz	Fastqsanger.gz
	SRR850659_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Enterobacter cloacae BWH 29

Project description:Enterobacter cloacae BWH 29 Genome sequencing and assembly

| PRJNA201969 | ENA

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 (Enterococcus, Staphylococcus, Klebsiella, Acinetobacter, Pseudomonas, and Enterobacter spp.) priority group with increasing multi-drug resistance via the acquisition of resistance plasmids. However, E. cloacae can also display forms of antibiotic refractoriness, such as heteroresistance and tolerance. Here, we report that E. cloacae displays transient heteroresistance to aminoglycosides, which is accompanied with the formation of small colony variants (SCVs) with increased minimum inhibitor concentration (MIC) of 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 SCV formation, pointing to its indispensable role in these processes. The introduction of a constitutively active allele of cpxA led to high aminoglycoside MICs, consistent with cell envelope stress response 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 in the ΔcpxRA mutant. Moreover, copper exposure also elevated the gentamicin MICs of clinical isolates from bloodstream infections, 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 cloacae subsp. cloacae

Project description:Enterobacter cloacae subsp. cloacae Genome sequencing and assembly

| PRJNA401340 | ENA

Enterobacter cloacae subsp. cloacae

Project description:Enterobacter cloacae subsp. cloacae Genome sequencing and assembly

| PRJNA362587 | ENA

Enterobacter cloacae subsp. cloacae

Project description:Enterobacter cloacae subsp. cloacae Genome sequencing and assembly

| PRJNA390433 | ENA

Enterobacter cloacae

Project description:Enterobacter cloacae Genome sequencing and assembly