Transcriptome of the NWMN_0641 deletion mutant strain and the wild-type Staphylococcus aureus Newman strain
Ontology highlight
ABSTRACT:
ORGANISM(S): Staphylococcus aureus subsp. aureus str. Newman
SUBMITTER: Lefu Lan
PROVIDER: E-GEOD-57260 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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:The S. aureus transcriptome was assessed for strains Newman (wild type) and Newman (sarZ) during both exponential (2hr) and early stationary (5hr) cell growth. The S. aureus transcriptome was assessed for strains Newman (wild type) and Newman (sarZ) during both exponential (2hr) and early stationary (5hr) cell growth. The experiment was performed in duplicate or triplicate, and RNA samples labeled/hybridized to independent commercially available Affymetrix GeneChips
2010-05-15 | E-GEOD-13138 | biostudies-arrayexpress
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:Membrane vesicles (MVs) are produced by species across all domains of life and have diverse physiological functions and promising applications. While the mechanisms for vesiculation in Gram-negative bacteria are well-established, the genetic determinant and regulation of MVs biogenesis in Gram-positive bacteria remain still largely unknown. Here, we demonstrate that a Q225P substitution in the alternative sigma factor SigB greatly triggers MVs production in Staphylococcus aureus strain Newman by directly repressing expression of alkaline shock protein 23, wherein the Q225P mutation hinders the specific binding of SigB to the asp23 promoter. Isogenic deletion of asp23 consistently promotes MVs formation in Newman, highlighting the critical role of both sigB and asp23 in modulating S. aureus vesiculation. While bacterial growth and cytoplasmic membrane fluidity do not be impaired, mutation of asp23 elicits a weakened cell wall and enhanced autolysis that potentially involved in LrgAB-controlled hydrolases and PSMα-mediated activities, which ultimately leads to hypervesiculation in Newman. Furthermore, TEM and proteomic analysis suggest nearly identical morphology and composition, but virulence-associated factors are significantly enriched in MVs upon asp23 deletion. Overall, this study reveals novel genetic determinants and cues underlying S. aureus vesiculation, advancing the understanding of the physiology of MVs biogenesis in Gram-positive bacteria.
2024-01-10 | PXD048184 | Pride
Project description:The alternative sigma factor M-OM-^CB of Staphylococcus aureus is involved in the coordination of the general stress response, expression of virulence determinants and modulation of antibiotic resistance levels. It controls a large regulon, either directly by recognizing conserved M-OM-^CB promoter sequences, or indirectly via M-OM-^CB-dependent elements. The M-OM-^CB-controlled yabJ-spoVG operon encodes two such putative downstream elements. We report here transcriptome analysis in S. aureus Newman showing that inactivation of the yabJ-spoVG operon had primarily a repressing effect on a small subregulon comprising mainly virulence factors, including a nuclease (nuc), a protease (splE) and a lipase (lip).. As a consequence extracellular nuclease, protease and lipase activities were reduced in a yabJspoVG mutant. Trans-complementation by SpoVG was sufficient to restore their reduced phenotypic expression and lowered transcription due to yabJ-spoVG deletion. It did not restore, however, the changes triggered by M-OM-^CB inactivation, indicating that both regulons do only partially overlap, despite the M-OM-^CB dependency of the yabJ-spoVG expression. Thus, M-OM-^CB is likely to control additional, SpoVG-independent factors affecting the expression of numerous hydrolytic enzymes. SpoVG, on the other hand, seems to fine-tune the M-OM-^CB-dependent regulation of a subset of virulence factors by antagonizing the M-OM-^CB effect. Newman wild type strain compared to double mutant spoVG and yabJ or to sigB truncated mutant
2011-11-23 | E-GEOD-30115 | biostudies-arrayexpress
Project description:Staphylococcus aureus is a leading cause of bloodstream infections worldwide. In the United States, many of these infections are caused by a strain known as USA300. Although progress has been made, our understanding of the S. aureus molecules that promote bacteremia and survival in human blood is incomplete. To that end, we analyzed the USA300 transcriptome during culture in human blood, human serum, and trypticase soy broth (TSB), a standard laboratory culture media. Notably, genes encoding several cytolytic toxins were up-regulated in human blood over time, and hlgA, hlgB, and hlgC (encoding gamma-hemolysin subunits HlgA, HlgB, and HlgC) were among the most highly up-regulated genes at all time points. Culture supernatants derived from a USA300 isogenic hlgABC-deletion strain (LAC?hlgABC) had significantly reduced capacity to form pores in human neutrophils and ultimately cause neutrophil lysis. Compared with the wild-type USA300 strain (LAC), LAC?hlgABC had modestly reduced ability to cause mortality in a mouse bacteremia model. On the other hand, wild-type and LAC?hlgABC strains caused virtually identical disease in a mouse skin infection model, and bacterial survival and neutrophil lysis after phagocytosis in vitro was similar between these strains. Comparison of the cytolytic capacity of culture supernatants from wild-type and isogenic deletion strains lacking hlgABC, lukS/F-PV (encoding PVL), and/or lukDE revealed significant functional redundancy among two-component leukotoxins in vitro. These findings may explain in part the apparent limited contribution of any single two-component leukotoxin to USA300 immune evasion and virulence. S. aureus strain USA300 transcriptome during culture in human blood, human serum, and trypticase soy broth (TSB): time course.
2011-08-25 | E-GEOD-25454 | 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 sigS gene in S. aureus encodes an ECF sigma factor. ECF sigma factors bind to core-RNA polymerase and redirecting promoter recognition to coordinate gene expression. To determine all of the genes in S. aureus whose expression is SigS dependent we preformed a microarray analysis of a wild type and sigS mutant strain. Genes showing altered expression levels in the sigS mutant versus the wild type were deemed SigS dependent. Two strains of S. aureus were used, the wild type RN4220 strain, and RN4220 containing a sigS mutation. Each strain was grown in triplicate, in TSB broth, at 37°C with shaking. The RN4220 sigS mutant has an increased lag phase. Therefore to synchronize cultures and isolate RNA from cells in the same phase of growth samples for microarray analysis were taken following 3 h growth of the wild type (which corresponds to a timepoint when sigS expression is at its highest) and 5 h growth of the sigS mutant.
2012-02-01 | E-GEOD-35336 | 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.
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Project description:The WalKR regulon was studied by comparing genes expression in a strain producing a constitutively active WalR regulator (WalRc) versus the wild type strain carrying the empty expression vector. Hybridizations were performed with three independent biological replicates. Our data allowed to identify 165 genes differentially expressed in the walRc expressing strain with a P-value M-bM-^IM-$ 0.05 using Z-test and a threshold value of two-fold change in transcriptional levels. Among them, 108 genes are activated, and 57 genes are repressed. About 10% of these results were confirmed by quantitative real time PCR, revealing the high reliability of this overall study. Beyond the major effect of the WalKR system on genes expressing cell wall hydrolases, we have shown that it activates a large number of genes involved in virulence, and probably through its positive impact on the SaeRS two-component system, is a major activator of S. aureus virulence. Cells were grown in TSB rich medium added with 0.25 M-BM-5M CdCl2 to allow walRc expression until OD600nm of 1. Gene expression was compared between the HG001 wild type reference strain carrying the pCN51 empty vector (HG001/pCN51) and the HG001 strain carrying a pCN51 derivative with the walRc allele under the control of the Pcad inducible promoter (HG001/pSD3-12). Each condition was done in triplicate and the data were analyzed using the Arraystat software. Genes were considered as differentially expressed if their transcriptional level differed by at least two-fold with a Z-test P-value M-bM-^IM-$ 0.05 in at least two of the replicates.
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