Long-read sequencing and phage typing of Enterococcus faecium
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB41626 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR4898532_1.fastq.gz | Fastqsanger.gz | |||
| ERR4898532_2.fastq.gz | Fastqsanger.gz | |||
| ERR4898533_1.fastq.gz | Fastqsanger.gz | |||
| ERR4898533_2.fastq.gz | Fastqsanger.gz |
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Project description:In this study, we aimed to further characterize Ern0160 functions and identify its targets. In silico prediction screen highlighted putative mRNA candidates. For two of them, homologous genes encoding for LysM-containing domain proteins (EFAU004_01059 and EFAU004_01150), we validated a direct and specific interaction to Ern0160. In addition, we found that Ern0160 overexpression was responsible for the repression of the target genes, emphasizing the mode of action of this sRNA. As a recent study provided the role of these genes in the virulence of E. faecium Aus0004 in a mouse model of systemic and urinary tract infections, we proposed that Ern0160 could be part of the regulatory network involved during colonization/infection by attenuating virulence. Furthermore, in vitro tests of antibiotic susceptibility profiles to vancomycin, teicoplanin, daptomycin, ciprofloxacin, and levofloxacin showed that a strain expressing Ern0160 presented lower MICs of fluoroquinolones compared to a ern0160-deleted strains. Very interestingly, we found that a gene implicated in fluoroquinolone resistance in E. faecium, Efmqnr was downregulated when Ern0160 was over-expressed, indicating a link between this sRNA and antibiotic resistance. For the first time, this study investigated throughout the identification of its cellular targets the regulation that could lead to virulence and fluoroquinolone resistance in E. faecium.
2025-01-01 | GSE239910 | GEO
Project description:Enterococcus faecium phage genome sequencing
| PRJNA704255 | ENA
Project description:BackgroundVancomycin-resistant enterococci (VRE) are successful nosocomial pathogens able to cause hospital outbreaks. In the Netherlands, core-genome MLST (cgMLST) based on short-read sequencing is often used for molecular typing. Long-read sequencing is more rapid and provides useful information about the genome's structural composition but lacks the precision required for SNP-based typing and cgMLST. Here we compared prophages among 50 complete E. faecium genomes belonging to different lineages to explore whether a phage signature would be usable for typing and identifying an outbreak caused by VRE. As a proof of principle, we investigated if long-read sequencing data would allow for identifying phage signatures and thereby outbreak-related isolates.ResultsAnalysis of complete genome sequences of publicly available isolates showed variation in phage content among different lineages defined by MLST. We identified phage present in multiple STs as well as phages uniquely detected within a single lineage. Next, in silico phage typing was applied to twelve MinION sequenced isolates belonging to two different genetic backgrounds, namely ST117/CT24 and ST80/CT16. Genomic comparisons of the long-read-based assemblies allowed us to correctly identify isolates of the same complex type based on global genome architecture and specific phage signature similarity.ConclusionsFor rapid identification of related VRE isolates, phage content analysis in long-read sequencing data is possible. This allows software development for real-time typing analysis of long-read sequencing data, which will generate results within several hours. Future studies are required to assess the discriminatory power of this method in the investigation of ongoing outbreaks over a longer time period.
| S-EPMC8542323 | biostudies-literature
Project description:Molecular Basis of Anderson Phage Typing Scheme
| PRJEB48030 | ENA
Project description:This study aims to determine the global gene expression in vancomycin resistant Enterococcus faecium (VRE) in response to a novel essential oil-vancomycin combination, and the individual components (vancomycin, carvacrol and cuminaldehyde) to help determine the mechanism of action of this antimicrobial formulation. This formulation increases the susceptibility of VRE to vancomycin and the array provides data on the synergistic mechanism of action. Five conditions (1. Control; 2. Carvacrol, 1.98 mM; 3. Cuminaldehyde, 4.20 mM; 4. Vancomycin, 0.031 mg/l; 5. Combination, 1.98 mM Carvacrol, 4.2 mM Cuminaldehyde, 0.031 mg/l vancomycin) all with 1% DMSO were tested in triplicate with a 60 minute exposure time before extraction.
2019-12-31 | E-MTAB-8072 | biostudies-arrayexpress
Project description:A set of small RNAs was identified in Vancomycin-resistant Enterococcus faecium, a leading cause of MDR infections. We described here the function of srn_2050, acting as a T-box riboswitch to regulate expression of downstream genes encoding the HisRS and AspRS aminoacyl-tRNA synthetases. Comparative RNAseq between Aus0004 and isogenic srn_2050 mutant identified the genes whose expression is impacted by the RNA. srn_2050 structure in its ‘off state’ was deciphered by in-line probing, containing T-box consensus sequences, a pseudoknot, a specifier loop and a terminator. Transcription binding assays between the riboswitch and either tRNAAsp or tRNAHis indicate that each deacylated tRNA interacts with the T-box. Their anticodons bind to a GACAC sequence within the specifier loop (GAC and CAC are Asp and His codons, respectively), whereas tRNATyr (UA/C-U) does not. A pioneering evaluation of E. faecium amino acid auxotrophy, with emphasis on E. faecium strain Aus0004, revealed auxotrophy for Histidine but not for Aspartic acid. Based on comparative growths and RNAseq between Aus004 and Aus004-srn2050, the riboswitch is shown essential for growth under aspartate starvation. This is the first example of a functional riboswitch in E. faecium with two overlapping codons allowing a dual tRNA-dependent regulation at transcriptional level.
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Project description:In our study, we employed activity-based protein profiling (ABPP), a technique that uses specialized inhibitors to identify active serine hydrolases in different strains of E. faecium (clade A1 and A2) and E. lactis under various growth conditions. Serine hydrolases, a large and diverse family of enzymes that include established drug targets like penicillin-binding proteins, have other less-studied subfamilies. In addition to fluorescent, gel-based profiling, we used a biotin-tagged fluorophosphonate probe for the enrichment and identification of serine hydrolase enzymes via streptavidin enrichment and liquid chromatography/mass spectrometry analysis. This led to the discovery of 11 largely unexplored potential targets (including α,β-hydrolases, SGNH-hydrolases, phospholipases, amidases, and peptidases) that could be exploited for drug developmentagainst the vancomycin-resistant E. faecium strain E745.
2024-06-22 | PXD048798 | Pride
Project description:The rise of antibiotic resistance and decline of antibiotic discovery urgently calls for novel mechanistic understanding of pharmacological and evolutionary interactions between antibiotics and multidrug resistant bacteria to revitalize existing antibiotics. The evolutionary cross-resistance to antibiotics has received intensive attention previously. Nevertheless, whether and how bacteria develop negative responses, under the selective pressure of antibiotics by inverting the evolutionary trajectory remains unclear. Here we found an instance of collateral sensitivity, in which clinical vancomycin-resistant Enterococcus faecium (VREfm) pathogens exhibit dramatic and specific susceptibility to pleuromutilin antibiotics, decreased minimal inhibitory concentrations (MICs) from 128 µg/mL to 0.03 µg/mL. The unique trade-off between vancomycin and pleuromutilins is mediated by the epistasis between the van gene cluster and msrC encoding an ABC-F protein protecting bacterial ribosomes. We validated the efficacy of pleuromutilins in vivo through reducing colonization and promoting microbiota restoration. Our findings provide an alternative approach to inverting the selective advantage and reversing the route of vancomycin resistance evolution, and to treat VREfm associated infections.
2022-05-20 | PXD030906 | Pride
Project description:Vancomycin-resistant Enterococcus faecium Genome sequencing
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