Pangenome analysis of S. aureus
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB56446 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR10308505_1.fastq.gz | Fastqsanger.gz | |||
| ERR10308505_2.fastq.gz | Fastqsanger.gz | |||
| ERR10308510_1.fastq.gz | Fastqsanger.gz | |||
| ERR10308510_2.fastq.gz | Fastqsanger.gz | |||
| ERR10308511_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 328 |
Similar Datasets
Project description:Staphylococcus aureus (S. aureus) is a known pathogen able to infect humans and animals. Human S. aureus isolates are often associated with carriage of Sa3int prophages combined with loss of beta-hemolysin production due to gene disruption, whereas animal isolates are positive for beta-hemolysin associated with absence of Sa3int prophages. Sa3int prophages are known to contribute to staphylococcal fitness and virulence in human host by providing human-specific virulence factors encoded on the prophage genome. Strain-specific differences in regard to phage transfer, lysogenization and induction are attributable to yet unknown staphylococcal factors specifically influencing prophage gene expression. In this work we used tagRNA-sequencing approach to specifically search for these unknown host factors and differences in prophage gene expression. For this purpose, we established a workflow revealing the first direct comparison for differential gene expression analysis on two distinct single-lysogenic S. aureus isolates. Further, global gene expression patterns were investigated in two S. aureus isolates upon mitomycin C treatment and compared to uninduced conditions. This provides new insights into the tightly linked host-phage interaction network.
2022-10-03 | GSE214523 | GEO
Project description:Understanding novel mechanism bacteria ustilize in the clinics to become resistant to antibiotics is critical. The study aims to identify genes associated with Vancomycin resistance. Clinical isolates from a single patient with increasing resistance to vancomycin were grown in the presence and absence of vancomycin.Staphylococcus aureus strain 2275 is the reference for this series. S. aureus isolates from a single patient were grown in the presence and absence of vancomycin over a 2 hour time course. RNA samples were extracted at 30, 60 90 and 120 minutes post exposure to antibiotic. Samples were hybridized on aminosilane coated slides with 70-mer oligos comparing mock treated and treated cells to the first strain isolated in the lineage. Differnetial gene expression patterns were determined.
2011-04-08 | E-GEOD-26353 | biostudies-arrayexpress
Project description:To explore whether S. aureus contributes to the mechanism of pain, we assayed S. aureus isolates from 3 severe pain PJI (sp-PJI) and 3 mild pain PJI (mp-PJI) by RNA-sequencing.
2025-05-20 | GSE203444 | GEO
Project description:Understanding novel mechanism bacteria ustilize in the clinics to become resistant to antibiotics is critical. The study aims to identify genes associated with Vancomycin resistance. Clinical isolates from a single patient with increasing resistance to vancomycin were grown in the presence and absence of vancomycin.Staphylococcus aureus strain 2275 is the reference for this series.
2011-04-08 | GSE26353 | GEO
Project description:To explore the difference in the expression profile of Staphylococcus aureus in chronic periprosthetic joint infection (C_PJI) and acute PJI (A_PJI), we assayed S. aureus isolates from 4 C_PJI and 4 A_PJI by RNA-sequencing.
2025-08-08 | GSE210722 | GEO
Project description:Microarray hybridization analysis was conducted to identify genes that may affect biofilm formation. Isolates from the 50 clinical isolates, two from LSG (strain number 2 and 7) and two from HSG donors (strain number 10 and 33) were selected. We monitored relative mRNA abundance in the four clinical S. aureus isolates using the Genechip S. aureus Genome Array (GeneChip Expression, Affymetrix, Inc., USA) to study the patterns of gene expression. The arrays contain probe sets corresponding to more than 3,300 S. aureus ORFs. Additionally, they contain probes to detect RNA of either forward or reverse orientation from more than 4,800 intergenic regions. In total, 107 were used as a control to verify the test results. A total of 432 probes on the microarrays overlapped between ORFs and intergenic regions. Two samples from each strains were used for the microarray and two independent experiments were performed.
2013-02-13 | E-GEOD-44268 | biostudies-arrayexpress
Project description:WalKR is an essential two component regulatory system in S. aureus, thought to control cell wall metabolism. Using genome sequencing of 5 paired clinical isolates of vancomycin-susceptible and vancomycin-intermediate S. aureus we found frequent, but unique, mutations in this locus. To investigate the contribution of these mutations to vancomycin resistance allelic replacement WalK (G223D) and WalR (K208R) mutants were generated and compared to the parent strains. Mutations in walk and walR led to increased vancomycin resistance, reduced biofilms formation and attenuation of virulence, demonstrating that minor genetic changes in this locus can lead to significant changes in bacterial resistance and virulence. Microarray transcriptional comparisons were performed to investigate the regulatory effects of the WalK (G223D) and WalR (K208R) mutations, and demonstrated that while changes in genes affecting cell wall metabolism were detected, more dramatic changes were found in regulation of cellular metabolism. Transcriptional profiling of laboratory derived S. aureus walKR mutants compared to the parent isolates. TPS3130 has a single point mutation in walK, and TPS3190 has a single point mutation in walR. Two condition experiment TPS3130 vs JKD6009 and TPS3190 vs JKD6004. 3 biological replicates per isolate pair, one replicate per slide.
2012-05-31 | E-GEOD-29157 | biostudies-arrayexpress
Project description:Transcriptional profiling of the small colony variant (SCV) S. aureus isolate (JKD6229) compared to the parent isolate with a normal phenotype (JKD6210). Both isolates were from a patient with persistent S. aureus infection, and the SCV strain arose during failed antibiotic therapy.
2010-08-13 | GSE20957 | GEO
Project description:Staphylococcus aureus is one of the first and most prevalent pathogens cultured from the airways of cystic fibrosis (CF) patients, which can persist there for extended periods. Airway infections in CF patients are characterized by a strong inflammatory response of highly recruited neutrophils. One killing mechanism of neutrophils is the formation of neutrophil extracellular traps (NETs), which capture and eradicate bacteria by extracellular fibers of neutrophil chromatin decorated with antimicrobial granule proteins. S. aureus secretes nuclease, which can degrade NETs. We hypothesized, that S. aureus adapts to the airways of CF patients during persistent infection by escaping from NET-mediated killing via an increase of nuclease activity. Sputum samples of CF patients with chronic S. aureus infection were visualized by confocal microscopy after immuno-fluorescence staining for NET-specific markers, S. aureus bacteria and overall DNA structures. Nuclease activity was analyzed in sequential isogenic long persisting S. aureus isolates, as confirmed by whole genome sequencing, from an individual CF patient using a FRET-based nuclease activity assay. Additionally, some of these isolates were selected and analyzed by qRT-PCR to determine the expression of nuc1 and regulators of interest. NET-killing assays were performed with clinical S. aureus isolates to evaluate killing and bacterial survival depending on nuclease activity. To confirm the role of nuclease during NET-mediated killing, a clinical isolate with low nuclease activity was transformed with a nuclease expression vector (pCM28nuc). Furthermore, two sputa from an individual CF patient were subjected to RNA-sequence analysis to evaluate the activity of nuclease in vivo. In sputa, S. aureus was associated to extracellular DNA structures. Nuclease activity in clinical S. aureus isolates increased in a time-and phenotype-dependent manner. In the clinical isolates, the expression of nuc1 was inversely correlated to the activity of agr and was independent of saeS. NET-mediated killing was significantly higher in S. aureus isolates with low compared to isolates with high nuclease activity. Importantly, transformation of the clinical isolate with low nuclease activity with pCM28nuc conferred protection against NET-mediated killing confirming the beneficial role of nuclease for protection against NETs. Also, nuclease expression in in vivo sputa was high, which underlines the important role of nuclease within the highly inflamed CF airways. In conclusion, our data show that S. aureus adapts to the neutrophil-rich environment of CF airways with increasing nuclease expression most likely to avoid NET-killing during long-term persistence.
2019-11-01 | GSE139662 | GEO
Project description:Staphylococcus aureus is a pulmonary pathogen associated with substantial human morbidity and mortality. As vaccines targeting virulence determinants have failed to be protective in humans, other factors are likely involved in pathogenesis. Here we analysed transcriptomic responses of human clinical isolates of S. aureus from initial and chronic infections. We observed upregulated collagenase and proline transporter gene expression in chronic infection isolates. Metabolomics of bronchiolar lavage fluid, fibroblast infection, growth assays and analysis of bacterial mutant strains showed that airway fibroblasts produce collagen during S. aureus infection. Host-adapted bacteria upregulate collagenase, which degrades collagen and releases proline. S. aureus then imports proline, which fuels oxidative metabolism via the tricarboxylic acid cycle. Proline metabolism provides host-adapted S. aureus with a metabolic benefit enabling out-competition of non-adapted strains. These data suggest that clinical settings characterized by airway repair processes and fibrosis provide a milieu that promotes S. aureus adaptation and supports infection.
2024-07-31 | GSE268637 | GEO