Stp1 and Stk1 regulated genes during S. aureus post-exponential phase growth
Ontology highlight
ABSTRACT:
ORGANISM(S): Staphylococcus aureus subsp. aureus COL Staphylococcus aureus
PROVIDER: GSE21426 | GEO | 2010/04/22
SECONDARY ACCESSION(S): PRJNA126381
REPOSITORIES: GEO
Similar Datasets
Project description:Genes that showed altered expression in Stk1 and Stp1 deficient Staphylococcus aureus Newman were identified. strain comparison, global regulation Deletion mutants were examined for alterations in gene expression.
2010-04-22 | E-GEOD-21426 | biostudies-arrayexpress
Project description:To study the roles of NWMN_0641, we used microarray to compare the transcriptome of the NWMN_0641 deletion strain with that of the wild-type Staphylococcus aureus Newman strain. Transcriptome of the NWMN_0641 deletion mutant strain and the wild-type Newman strain
2014-11-04 | GSE57260 | GEO
Project description:To study the roles of NWMN_0641, we used microarray to compare the transcriptome of the NWMN_0641 deletion strain with that of the wild-type Staphylococcus aureus Newman strain. Transcriptome of the NWMN_0641 deletion mutant strain and the wild-type Newman strain We sought to obtain the transcriptomes of the NWMN_0641 deletion mutant strain and the wild-type Newman strain when bacteria were grown TSB medium (without glucose)
2014-11-04 | E-GEOD-57260 | biostudies-arrayexpress
Project description:The SaeRS two-component regulatory system of Staphylococcus aureus is known to affect the expression of many genes. The SaeS protein is the histidine kinase responsible for phosphorylation of the response regulator SaeR. In S. aureus Newman, the sae system is constitutively expressed due to a point mutation in saeS, relative to other S. aureus strains, which results in substitution of proline for leucine at amino acid 18. Strain Newman is unable to form a robust biofilm and we report here that the biofilm-deficient phenotype is due to the saeSP allele. Replacement of the Newman saeSP with saeSL, or deletion of saeRS, resulted in a biofilm-proficient phenotype. Newman culture supernatants were observed to inhibit biofilm formation by other S. aureus strains, but did not affect biofilm formation by S. epidermidis. Culture supernatants of Newman saeSL or Newman ΔsaeRS had no significant effect on biofilm formation. The inhibitory factor was inactivated by incubation with proteinase K, but survived heating, indicating that the inhibitory protein is heat-stable. The inhibitory protein was found to affect the attachment step in biofilm formation, but had no effect on preformed biofilms. Replacement of saeSL with saeSP in the biofilm-proficient S. aureus USA300 FPR3757 resulted in the loss of biofilm formation. Culture supernatants of USA300 FPR3757 saeSP, did not inhibit biofilm formation by other staphylococci, suggesting that the inhibitory factor is produced but not secreted in the mutant strain. A number of biochemical methods were utilized to isolate the inhibitory protein. Although a number of candidate proteins were identified, none were found to be the actual inhibitor. In an effort to reduce the number of potential inhibitory genes, RNA-Seq analyses were done with wild-type strain Newman and the saeSL and ΔsaeRS mutants. RNA-Seq results indicated that sae regulates many genes that may affect biofilm formation by Newman.
2015-04-30 | GSE65827 | GEO
Project description:The Staphylococcus aureus Panton Valentine leukocidin (PVL) is a pore-forming toxin secreted by strains epidemiologically associated with the current outbreak of community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and with the often lethal necrotizing pneumonia. To investigate the role of PVL in pulmonary disease, we tested the pathogenicity of clinical isolates, isogenic PVL-negative and PVL-positive S. aureus strains, as well as purified PVL, in a mouse acute pneumonia model. Here we show that PVL is sufficient to cause pneumonia and that the expression of this leukotoxin induces global changes in transcriptional levels of genes encoding secreted and cell-wall-anchored staphylococcal proteins, including the lung inflammatory factor staphylococcal protein A (Spa). Keywords: comparative transcription profile in the presence or absence of PVL toxin
2007-02-13 | GSE6985 | GEO
Project description:Staphylococcus aureus is a Gram-positive human pathogen causing a variety of human diseases in both hospital and community settings. This bacterium is so closely associated with prophages that it is rare to find S. aureus isolates without prophages. Two phages are known to be important for staphylococcal virulence: the beta-hemolysin (hlb) converting phage and the Panton-Valentine Leukocidin (PVL) converting phage. The hlb-converting phage is found in more than 90% of clinical isolates of S. aureus. This phage produces exotoxins and immune modulatory molecules, which inhibit human innate immune responses. The PVL-converting phage produces the two-component exotoxin PVL, which can kill human leucocytes. This phage is wide-spread among community-associated methicillin resistant S. aureus (CA-MRSA). It also shows strong association with soft tissue infections and necrotizing pneumonia. Several lines of evidence suggest that staphylococcal prophages increase bacterial virulence not only by providing virulence factors but also by altering bacterial gene expression: 1) Transposon insertion into prophage regulatory genes, but not into the genes of virulence factors, reduced S. aureus killing of Caenorhabditis elegans.; 2) Although the toxins and immune modulatory molecules encoded by the hlb- converting phages do not function in the murine system, deletion of NM3, the hlb-converting phage in S. aureus Newman, reduced staphylococcal virulence in the murine abscess formation model. 3) In a preliminary microarray experiment, prophages in S. aureus Newman altered the expression of more than 300 genes. In this research proposal, using microarray and high-throughput quantitative RT-PCR (qRT-PCR) technologies, we will identify the effects of the two important staphylococcal phages on the gene expression of S. aureus in both in vitro and in vivo conditions. This project is intended to be completed within one year. All the data – microarray, qRT-PCR and all the primer sequences- will be made available to public 6 month after completion. Data from this project will help us to understand the role of prophages in the S. aureus pathogenesis and can lead to development of a strategy to interfere with the pathogenesis process. Staphylococcus aureus subsp.aureus strain Newman (reference) and Staphylococcus aureus subsp.aureus strain Newman yhcR knockout(query) were grown in TSA broth.Samples were grown under aerobic and anaerobic conditions and RNA samples harvested at mid log, stationary, and log phases.Samples were hybridized on aminosilane coated slides with 70-mer oligos.
2011-12-31 | E-GEOD-26585 | biostudies-arrayexpress
Project description:BRcells and DRcells show distinct transcriptomic profiles. We assessed transcriptome changes, by deep-sequencing, of different subpopulations of Staphylococcus aureus strain Newman from multicellular aggregates.
2017-11-01 | GSE69835 | GEO
Project description:Array analysis of total RNA from broncho-alveolar lavage (BAL) from mice infected with influenza virus (PR8) and/or Staphylococcus aureus (Newman)
2016-09-01 | GSE83359 | GEO
Project description:Staphylococcus aureus Newman and Staphylococcus epidermidis Tu3298, 20 minutes post challenge with sub-inhibitory concentration of sapienic acid vs equivalent concentration of ethanol. Challenge was added at mid logarithmic growth (OD600 0.5). Biological triplicates of samples were sequenced.
2016-07-31 | E-MTAB-4587 | biostudies-arrayexpress
Project description:Staphylococcus aureus is an important human pathogen causing skin infection and many serious diseases such as pneumonia, sepsis, and toxic shock syndrome. In the bacterium, the membrane-bound protease FtsH plays important roles in the bacterial resistance to various stresses. This study was initiated to explain the strain-specific aggregation of the ftsH-deletion mutant of the Newman strain. To understand the molecular basis of the phenotype, we identified FtsH substrate proteins by comparing the protein contents of two different strains, Newman and USA300, and found that, in the strain Newman, a single nucleotide change in the sensor histidine kinase saeS gene placed the SaeRS two-component system under the control of FtsH, leading to the strain-specific cell-aggregation phenotype. Not only does our study provide a new methodology for protease-substrate determination but it also demonstrates that even a single nucleotide polymorphism can rewire bacterial regulatory network, resulting in a strain-specific phenotype. Our study shows the pitfall of making sweeping conclusion based on experimental results from a single bacterial strain.
2017-09-15 | GSE89791 | GEO