Ontology highlight
ABSTRACT:
PROVIDER: PRJNA836617 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19148707_1.fastq.gz | Fastqsanger.gz | |||
| SRR19148707_2.fastq.gz | Fastqsanger.gz | |||
| SRR19148708_1.fastq.gz | Fastqsanger.gz | |||
| SRR19148708_2.fastq.gz | Fastqsanger.gz | |||
| SRR19148709_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 70 |
Similar Datasets
Project description:In many pathogens, quorum-sensing systems regulate virulence. Quorum-sensing is therefore often proposed as a target for antivirulence drug development. Coagulase-negative staphylococci are leading causes of nosocomial blood infections and of mortality due to sepsis as the most extreme consequence of such infections. However, there is a severe lack of understanding how virulence and especially quorum-sensing affects coagulase-negative staphylococcal sepsis. Using a mouse systemic infection model, we here show that the staphylococcal Agr quorum-sensing system has a strong impact on mortality from sepsis caused by the exemplary coagulase-negative staphylococcal species Staphylococcus haemolyticus. To that end, we analyzed the mechanism and regulon of S. haemolyticus Agr, which revealed a strong focus of quorum-sensing regulation of phenol-soluble modulin toxins. Our results further indicate that PSMs are the virtually exclusive mediators of the Agr effect on S. haemolyticus sepsis and suggest that the predominant underlying mechanism is cytolytic capacity of PSMs. These findings imply that Agr and PSMs represent promising targets for antivirulence drug development targeting sepsis caused by coagulase-negative staphylococci. This contrasts quorum-sensing targeted efforts to control S. aureus blood infections, for which such approaches are considered less promising - a difference our results suggest is due to the much more focused role of Agr control in coagulase-negative staphylococci, where among toxins, Agr exclusively and exceptionally tightly controls PSMs.
2025-09-23 | GSE285447 | GEO
Project description:Staphylococcus haemolyticus is a skin commensal emerging as an opportunistic pathogen. Nosocomial isolates of S. haemolyticus are the most antibiotic resistant members of the coagulase negative staphylococci (CoNS), but information about other S.haemolyticus virulence factors is scarce. Bacterial virulence is mediated by membrane vesicles (MVs) which enable secretion and long distance delivery of bacterial effector molecules while protecting the cargo from proteolytic degradation from the environment. We wanted to determine if the MV protein cargo of S.haemolyticus is strain specific and enriched in certain MV associated proteins compared to the totalsecretome. The present study shows that both clinical and commensal S. haemolyticus isolates produce membrane vesicles. The MV cargo of both strains was enriched in proteins involved in adhesion and in acquisition of iron. The MV cargo of the clinical strain was further enriched in antimicrobial resistance proteins.
2018-11-30 | PXD010389 | Pride
Project description:We have conducted a genome-wide analysis of spontaneous copy number variation (CNV) in the laboratory mouse. We used high resolution microarrays to identify 38 CNVs between 14 colonies of the C57BL/6 strain spanning ~967 generations of inbreeding, and examined these loci in 12 additional strains. It is clear from our results that many CNVs arise through a highly non-random process: 18 of 38 were the product of recurrent mutation, and rates of change vary roughly four orders of magnitude across different loci. These recurrent CNVs are distributed throughout the genome, affect 43 genes, and fluctuate in copy number over mere hundreds of generations, observations that raise questions about their contribution to natural variation. Keywords: Representational oligonucleotide microarray analysis, comparative genomic hybridization, DNA copy number variation, structural variation, inbred mice, spontaneous mutation rate
2007-10-28 | GSE8980 | GEO
Project description:We have conducted a genome-wide analysis of spontaneous copy number variation (CNV) in the laboratory mouse. We used high resolution microarrays to identify 38 CNVs between 14 colonies of the C57BL/6 strain spanning ~967 generations of inbreeding, and examined these loci in 12 additional strains. It is clear from our results that many CNVs arise through a highly non-random process: 18 of 38 were the product of recurrent mutation, and rates of change vary roughly four orders of magnitude across different loci. These recurrent CNVs are distributed throughout the genome, affect 43 genes, and fluctuate in copy number over mere hundreds of generations, observations that raise questions about their contribution to natural variation. Keywords: comparative genomic hybridization, DNA copy number variation, structural variation, inbred mice, spontaneous mutation rate
2007-10-28 | GSE8885 | GEO
Project description:Staphylococcus haemolyticus Genome sequencing
| PRJNA576986 | ENA
Project description:Staphylococcus haemolyticus Genome sequencing
| PRJNA551923 | ENA
Project description:Staphylococcus haemolyticus Sh29/312
| PRJNA279511 | ENA