Butyricimonas faecalis strain:H184
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ABSTRACT:
PROVIDER: PRJNA494677 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Gene content in various Enterococcus faecalis strains compared to E. faecalis V583. Strains have been compared to the V583 strain by comparative genomic hybridization using genome-wide PCR-based microarrays representing the V583 genome. Genes have been deemed "present" or "divergent" in the various strains.
2007-01-15 | E-MEXP-931 | biostudies-arrayexpress
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Project description:To further investigate the homeostatic response of E. faecalis to Fe exposure, we examine the whole-genome transcriptional response of wild-type (WT) exposed to non toxic Fe excess. This experiment correspond the work titled Transcriptomic response of Enterococcus faecalis to iron excess (work in preparation) A four chip study using total RNA recovered from four separate wild-type cultures of Enterococcus faecalis OG1RF, two controls samples (N medium growth) and two iron samples (N medium gowth with 0.5 mM Fe-NTA). Each chip measures the expression level of 3,114 genome genes from Enterococcus faecalis strain V583 (A7980-00-01).
2012-03-01 | E-GEOD-34432 | biostudies-arrayexpress
Project description:Transcriptional profiling of E. faecalis E99 WT and an isogenic ΔperA strain grown in THB + 1% glucose. Pathogenic E. faecalis are enriched for a pathogenicity island (PAI). This 150-kb island harbors a number of well characterized virulence genes plus a number of determinants of unknown function including one encoding a transcriptional regulator, designated PerA. In this work, we show that PerA coordinately regulates both metabolic and virulence genes, and influences the platelet binding ability of E. faecalis. Finally, we show that PerA responds to bicarbonate, an intestinal ion frequently used by pathogens to determine the site of infection. Together, these results indicate that PerA is a global transcriptional regulator that coordinately regulates genes responsible for enterococcal pathogenicity. These findings highlight a novel feature of PAI-mediated virulence regulation, namely the coordinate regulation of metabolic and virulence factors in the core genome by a horizontally acquired PAI-encoded transcriptional regulator.
2012-08-16 | GSE31538 | GEO
Project description:Enterococcus faecalis is commonly isolated from different wound types. However, despite its prevalence, the pathogenic mechanisms of E. faecalis during wound infections remain poorly understood. We adopted an in vivo E. faecalis transposon sequencing and RNA sequencing approach to identify fitness determinants that are crucial for replication and persistence of E. faecalis during wound infections in a mouse model. We demonstrated that E. faecalis purine biosynthesis genes are important for replication as purine metabolites are low in wounds during the early phase of wound infections. Furthermore, we found that the E. faecalis MptABCD phosphotransferase system (PTS) involved in the uptake of galactose and mannose, is crucial for E. faecalis persistence in wounds, and that carbohydrate availability changes as the infection progresses. To understand how MptABCD PTS contributes to the reduced fitness observed during E. faecalis wound persistence, we performed an in vitro transcriptomic analysis using the galactose/mannose PTS gene deletion mutant (∆mptD). When mannose was the sole carbohydrate source, shikimate and purine biosynthesis genes in the ∆mptD mutant were downregulated compared to the isogenic wild-type strain, indicating that mannose transport is interconnected with shikimate and purine biosynthesis. Together, our results suggest that dynamic and temporal microenvironment changes at the wound site affects pathogenic requirements and mechanisms of E. faecalis during infections and raise the possibility of inhibiting purine biosynthesis and/or MptABCD PTS to control wound infections.
2023-11-06 | GSE206750 | GEO
Project description:Enterococcus faecalis is commonly isolated from different wound types. However, despite its prevalence, the pathogenic mechanisms of E. faecalis during wound infections remain poorly understood. We adopted an in vivo E. faecalis transposon sequencing and RNA sequencing approach to identify fitness determinants that are crucial for replication and persistence of E. faecalis during wound infections in a mouse model. We demonstrated that E. faecalis purine biosynthesis genes are important for replication as purine metabolites are low in wounds during the early phase of wound infections. Furthermore, we found that the E. faecalis MptABCD phosphotransferase system (PTS) involved in the uptake of galactose and mannose, is crucial for E. faecalis persistence in wounds, and that carbohydrate availability changes as the infection progresses. To understand how MptABCD PTS contributes to the reduced fitness observed during E. faecalis wound persistence, we performed an in vitro transcriptomic analysis using the galactose/mannose PTS gene deletion mutant (∆mptD). When mannose was the sole carbohydrate source, shikimate and purine biosynthesis genes in the ∆mptD mutant were downregulated compared to the isogenic wild-type strain, indicating that mannose transport is interconnected with shikimate and purine biosynthesis. Together, our results suggest that dynamic and temporal microenvironment changes at the wound site affects pathogenic requirements and mechanisms of E. faecalis during infections and raise the possibility of inhibiting purine biosynthesis and/or MptABCD PTS to control wound infections.
2023-11-06 | GSE206749 | GEO