Evolutionary origins of the emergent ST796 clone of vancomycin resistant Enterococcus faecium
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB14733 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR1744890_1.fastq.gz | Fastqsanger.gz | |||
| ERR1744890_2.fastq.gz | Fastqsanger.gz | |||
| ERR1744891_1.fastq.gz | Fastqsanger.gz | |||
| ERR1744891_2.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 19 |
Similar Datasets
Project description:From early 2012, a novel clone of vancomycin resistant Enterococcus faecium (assigned the multi locus sequence type ST796) was simultaneously isolated from geographically separate hospitals in south eastern Australia and New Zealand. Here we describe the complete genome sequence of Ef_aus0233, a representative ST796 E. faecium isolate. We used PacBio single molecule real-time sequencing to establish a high quality, fully assembled genome comprising a circular chromosome of 2,888,087 bp and five plasmids. Comparison of Ef_aus0233 to other E. faecium genomes shows Ef_aus0233 is a member of the epidemic hospital-adapted lineage and has evolved from an ST555-like ancestral progenitor by the accumulation or modification of five mosaic plasmids and five putative prophage, acquisition of two cryptic genomic islands, accrued chromosomal single nucleotide polymorphisms and a 80 kb region of recombination, also gaining Tn1549 and Tn916, transposons conferring resistance to vancomycin and tetracycline respectively. The genomic dissection of this new clone presented here underscores the propensity of the hospital E. faecium lineage to change, presumably in response to the specific conditions of hospital and healthcare environments.
| S-EPMC5267571 | biostudies-literature
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:Preliminary analysis on extracts (pellets and supernatant) of vancomycin-resistant Enterococcus faecium strains cultured in BHI media. Untargeted LC-MS/MS acquisition performed in positive ion mode.
| MSV000092864 | GNPS
Project description:The enterococci comprise a genus of 49 low-GC content Gram-positive commensal species within the Firmicutes phylum that are known to occupy diverse habitats, notably the gastrointestinal core microbiota of nearly every phylum, including human. Of particular clinical relevance are two rogue species of enterococci, Enterococcus faecalis and the distantly related Enterococcus faecium, standing among the nefarious multi-drug resistant and hospital-acquired pathogens. Despite increasing evidence for RNA-based regulation in the enterococci, including regulation of virulence factors, their transcriptome structure and arsenal of regulatory small sRNAs (sRNAs) are not thoroughly understood. Using dRNA-seq, we have mapped at single-nucleotide resolution the primary transcriptomes of E. faecalis V583 and E. faecium AUS0004. We identified 2517 and 2771 transcription start sites (TSS) in E. faecalis and E. faecium, respectively. Based on the identified TSS, we created a global map of s70 promoter motifs. We also revealed features of 5’ and 3’UTRs across the genomes. The transcriptome maps also predicted 150 and 128 sRNA candidates in E. faecalis and E. faecium, respectively, some of which have been identified in previous studies and many of which are new. Finally, we validated several of the predicted sRNAs by Northern Blot in biologically relevant conditions. Comprehensive TSS mapping of two representative strains will provide a valuable resource for the continued development of RNA biology in the Enterococci.
2020-11-25 | GSE115009 | GEO
Project description:Grad-seq in Enterococcus faecalis V583 and Enterococcus faecium AUS004.
2022-11-28 | PXD031577 | Pride
Project description:Proteomic Characterization of Bacteriocin-Producing Enterococcus faecium Strains from foodstuffs
2023-03-11 | PXD037241 | Pride
Project description:Proteomic analysis Enterococcus faecium samples to assess proteomic alterations (20220922_NSco_Stinear)
2024-08-15 | PXD039831 | Pride
Project description:The transcriptome of Enterococcus faecium E1162 growing in Brain heart Infusion Broth was compared in the mid-exponential growth phase (A660 = 0.3) at 25 C and 37 C.
2013-09-01 | E-MEXP-3941 | biostudies-arrayexpress
Project description:Parkinson's disease (PD) is characterized by motor and non-motor symptoms, including muscle atrophy, bone deterioration, and neurodegeneration, largely attributed to dopamine depletion. However, the molecular mechanisms underlying brain, muscle, and bone dysfunctions in patients with PD remain poorly understood. This study explored gene expression patterns associated with neuroinflammation, muscle degeneration, and osteoblastogenesis and to evaluate the therapeutic potential of Enterococcus faecium FBL1 supplementation. En. faecium FBL1 significantly improved motor function and attenuated α-synuclein aggregation in the brain and muscle. Key markers of skeletal muscle differentiation (Myf5, MyoG, Myh1), osteoblastogenesis (Bmp2, Bmp4, SMAD1/5/8, RUNX2), and neurogenesis (Wnt3a, β-catenin, TCF1, LEF1) were downregulated in MPTP-induced PD but restored by En. faecium FBL1. This study highlights the pivotal role of osteoblastogenic (BMP/SMAD signaling) and neurogenic (Wnt signaling) pathways in maintaining muscle and bone homeostasis in PD. En. faecium FBL1 offers a novel therapeutic approach targeting the BMP/SMAD and Wnt signaling pathways to mitigate muscle and bone degeneration in patients with PD.
2024-12-22 | GSE284676 | GEO
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.
2020-11-16 | GSE161499 | GEO