Staphylococcus aureus
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ABSTRACT:
PROVIDER: PRJNA97993 | ENA |
REPOSITORIES: ENA
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Project description:We present a general overview of the changes in the genetic expression along a time curve through the first 20 minutes after acidification to pH 4.5 of exponentially growing cultures of the food pathogenic strain Staphylococcus aureus 50583. A newly developed method for statistical significance testing was used to detect significant gene expression responses. Most responses showed an increase or decrease from time zero to 10 minutes after acidification and then generally a stabilisation in expression level from 10 to 20 min. Increased urease activity appeared to be an important factor in the acid defence along with proton excretion by NADH dehydrogenase and macromolecule repair mechanisms. Oxidative stress responses such as increased expression of thioredoxin genes and upregulation of pentose phosphate pathway genes to generate more reducing power were also induced. A general reduction in the expression of genes encoding ribosomal proteins and genes involved in nucleotide synthesis as well as fatty acid and lipoprotein metabolism reflected the lowered growth rate after acidification. The pH shock did not appear to trigger major virulence responses or biofilm formation. The metal ion regulation and transport was affected by the acid shock and production of several cofactors such as molybdopterin was increased. Many of the presented observations could be explained, while some represent still unknown mechanisms. The patterns of regulation were confirmed by real time reverse transcriptase PCR. Together these results showed the main responses of S. aureus and will be a good starting point for future more specific in-depth studies of specific gene responses in conjunction with acid stress defence of S. aureus. Keywords: Time course, stress response
2007-07-29 | GSE7273 | GEO
Project description:Staphylococcus aureus is a leading cause of hospital- and community-associated infections. The organism’s ability to cause disease can, in part, be attributable to its ability to adapt to otherwise deleterious host-associated stresses. Like other bacterial species, the modulation of mRNA turnover appears to play an important role in S. aureus adaptation to certain environmental stresses. In the current study Affymetrix GeneChips® were used to examine the S. aureus responses to acid and alkaline shock-inducing conditions and to assess whether stress dependent changes in mRNA turnover are likely to facilitate the organism’s ability to tolerate extreme pH challenge. Results indicate that S. aureus adapts to pH shock by eliciting responses expected of organisms coping with pH alteration, including neutralizing cellular internal pH, DNA repair, amino acid biosynthesis and virulence factor expression. Further, it was found that the cellular response to alkaline conditions elicits a transcriptional profile that is similar to that of stringent response induced cells. Consistent with that observation, we show that the activator of the stringent response, (p)ppGpp, levels are profoundly elevated during alkaline shock conditions. We also show that the mRNA turnover properties of acid or alkaline shocked cells significantly differ from that of cells grown at neutral pH. A comparison of the mRNA degradation properties of transcripts whose titers either increased or decreased in response to sudden pH change revealed that alterations in mRNA degradation may, in part, account for the changes in the mRNA levels of factors predicted to mediate pH tolerance. Finally, a set of small stable RNA molecules were induced in response to acid or alkaline shock conditions. As in other organisms, these molecules may mediate mRNA stability and adaptation to otherwise deleterious growth conditions. Staphylococcus aureus strain UAMS-1 was grown to exponential phase and either mock treated (pH maintained at 7.4) or subjected to acid (pH 4)- or alkaline (pH 10) conditions for 30 min. Next, 200 micrograms per ml of rifampicin were added to arrest transcript synthesis. RNA was extracted from cell suspensions at 0, 2.5, 5, 15, and 30 min post-transcriptional arrest, labeled and hybridized to S. aureus GeneChips. A comparison of 0 min samples allowed assessment of acid and alkaline shock responses. A comparison of 0 min to that of various post-transcriptional arrest RNA samples allowed assessment of the mRNA turnover properties of mock vs acid or alkaline shocked cells. Duplicates of each experimental condition and corresponding post-transcriptional arrest time point were used (biological replicates).
2010-10-01 | E-GEOD-22233 | biostudies-arrayexpress
Project description:Genome-wide transcriptional profiling studies of the growth of bacteria with antimicrobial agents often reveals aspects of the drug-specific protective bacterial response. Fusidic acid is a steroid antimicrobial that inhibits protein synthesis by interfering with the release of elongation factor G (EF-G) after it has functioned in the translocation step. Two hundred and seventy two genes were both up- and down-regulated in a fusidic acid-susceptible strain of Staphylococcus aureus following challenge with 2 mg/L-1 fusidic acid for 15 min. Many genes altered by fusidic acid challenge are associated with protein synthesis such as fusA, which encodes EF-G which was up-regulated following exposure to the drug. The Staphylococcus microarray meta-database which curates and compares S. aureus transcriptome data revealed that the fusidic acid stimulon has the greatest overlap with the S. aureus cold shock- and stringent-responses. Six out of 9 autolysin genes making up the two component YycFG regulon (ssaA1-ssaA4, isaA and sceD) were also upregulated by fusidic acid; as were a carboxylesterase (est) and two putative Emr-Qac-like multidrug efflux pumps (emr-qac1 and emr-qac2). Genes down-regulated by fusidic acid induction encode a putative secreted acid phosphatase (sapS) and a number of protease genes (yjbG1, yjbG2, htrA1 and htrA2). Transcriptional analysis in conjunction with mutant fusidic acid susceptibility experiments revealed that th45 e virulence gene regulatory agr operon, a YycFG controlled peptidoglycan hydrolase gene isaA and the proteases htrA1 and htrA2 are required for the expression of wild-type levels of fusidic acid susceptibility.
2008-08-25 | GSE12210 | GEO
Project description:In the present study, we employed Affymetrix Staphylococcus aureus GeneChip arrays to investigate the dynamics of global gene expression profiles during the cellular response of Staphylococcus aureus to peracetic acid, which involved initial growth inhibition and subsequent partial recovery. Keywords: Time course
2006-05-31 | GSE4184 | GEO
Project description:Staphylococcus aureus is an important food poisoning bacterium. In food preservation, acidification is a well-known method. Permeant weak organic acids, like lactic and acetic acids, are known to be more effective against bacteria than inorganic strong acids (e.g., HCl). Growth experiments and metabolic and transcriptional analyses were used to determine the responses of a food pathogenic S. aureus strain exposed to lactic acid, acetic acid, and HCl at pH 4.5. Lactic and acetic acid stress induced a slower transcriptional response and large variations in growth patterns compared with the responses induced by HCl. In cultures acidified with lactic acid, the pH of the medium gradually increased to 7.5 during growth, while no such increase was observed for bacteria exposed to acetic acid or HCl. Staphylococcus aureus increased the pH in the medium mainly through accumulation of ammonium and the removal of acid groups, resulting in increased production of diacetyl (2,3-butanedione) and pyrazines. The results showed flexible and versatile responses of S. aureus to different types of acid stress. As measured by growth inhibition, permeant organic acid stress introduced severe stress compared with the stress caused by HCl. Cells exposed to lactic acid showed specific mechanisms of action in addition to sharing many of the mechanisms induced by HCl stress. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-87
2011-04-15 | E-BUGS-87 | biostudies-arrayexpress
Project description:Staphylococcus aureus is a leading cause of hospital- and community-associated infections. The organism’s ability to cause disease can, in part, be attributable to its ability to adapt to otherwise deleterious host-associated stresses. Like other bacterial species, the modulation of mRNA turnover appears to play an important role in S. aureus adaptation to certain environmental stresses. In the current study Affymetrix GeneChips® were used to examine the S. aureus responses to acid and alkaline shock-inducing conditions and to assess whether stress dependent changes in mRNA turnover are likely to facilitate the organism’s ability to tolerate extreme pH challenge. Results indicate that S. aureus adapts to pH shock by eliciting responses expected of organisms coping with pH alteration, including neutralizing cellular internal pH, DNA repair, amino acid biosynthesis and virulence factor expression. Further, it was found that the cellular response to alkaline conditions elicits a transcriptional profile that is similar to that of stringent response induced cells. Consistent with that observation, we show that the activator of the stringent response, (p)ppGpp, levels are profoundly elevated during alkaline shock conditions. We also show that the mRNA turnover properties of acid or alkaline shocked cells significantly differ from that of cells grown at neutral pH. A comparison of the mRNA degradation properties of transcripts whose titers either increased or decreased in response to sudden pH change revealed that alterations in mRNA degradation may, in part, account for the changes in the mRNA levels of factors predicted to mediate pH tolerance. Finally, a set of small stable RNA molecules were induced in response to acid or alkaline shock conditions. As in other organisms, these molecules may mediate mRNA stability and adaptation to otherwise deleterious growth conditions.
2010-10-01 | GSE22233 | GEO
Project description:Bacterial persister cells are phenotypic variants that exhibit a transient non-growing state and antibiotic tolerance. Here we provide in vitro evidence of Staphylococcus aureus persisters within infected host cells. We show that the bacteria surviving antibiotic treatment within host cells are persisters, displaying biphasic killing and reaching a uniformly non-responsive, non-dividing state when followed at the single-cell level. This phenotype is stable but reversible upon antibiotic removal. Intracellular S. aureus persisters remain metabolically active, but display an altered transcriptomic profile consistent with activation of stress responses, including the stringent response as well as cell-wall stress, SOS and heat-shock responses. These changes are associated with multidrug tolerance after exposure to a single antibiotic. We hypothesize that intracellular S. aureus persisters may constitute a reservoir for relapsing infection, and could contribute to therapeutic failures.
2020-03-25 | GSE139659 | 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:Previous evaluation by different molecular and physiological assays of Staphylococcus aureus (S. aureus) responses to heat shock exposure yielded a still fragmentary view of the mechanisms determining bacterial survival or death at supra-physiological temperatures. This study analyzed diverse facets of S. aureus heat-shock adjustment by recording global transcriptomic and metabolic responses of bacterial cultures shifted for 10 min from 37oC to a sub-lethal (43oC) or eventually lethal (48oC) temperature. A relevant metabolic model of the combined action of specific stress response mechanisms with more general, energy-regulating metabolic pathways in heat-shocked S. aureus was designed. While S. aureus cultures shifted to 43oC or left at 37oC showed marginal differences in growth and survival rates, bacterial cultures exposed to 48oC showed a rapid growth arrest followed by a subsequent decline in viable counts. The most substantial heat shock-induced changes at both 43oC and 48oC occurred in transcript levels of HrcA- and CtsR-regulated genes, encoding classical chaperones DnaK and GroESL, and some Hsp100/Clp ATPases components, respectively. Other metabolic pathways up-regulated by S. aureus exposure at 48oC included genes encoding several enzymes coping with oxidative stress, and DNA damage, or/and impaired osmotic balance. Some major components of the pentose phosphate cycle and gluconeogenesis were also up-regulated, which reflected depletion of free glucose by bacterial cultures grown in Mueller-Hinton broth prior to heat shock. In contrast, most purine- and pyrimidine-synthesis pathway components and amino acyl-tRNA synthetases were down-regulated at 48oC, as well as arginine deiminase and major fermentative pathway components, such as alcohol, lactate and formate dehydrogenases. Despite the heat-induced, increased requirements for ATP-dependent macromolecular repair mechanisms combined with declining energy sources, intracellular ATP levels remained remarkably constant during heat shock. In conclusion, the sequential loss of replication and viability at 48oC cannot be explained by significant reductions in intracellular ATP levels, but may reflect ATP rerouting for macromolecular repair mechanisms and cell survival. Our metabolic model also suggests that heat-stressed S. aureus should down-regulate the production of potential, DNA-damaging reactive oxygen species that might result from electron transport-generated ATP, involving excessive levels of free heavy metals, in particular iron. Keywords: Staphylococcus aureus; heat shock; stress responses; transcriptomic profiling; physiological adjustment
2009-04-22 | GSE12920 | GEO
Project description:Previous evaluation by different molecular and physiological assays of Staphylococcus aureus (S. aureus) responses to heat shock exposure yielded a still fragmentary view of the mechanisms determining bacterial survival or death at supra-physiological temperatures. This study analyzed diverse facets of S. aureus heat-shock adjustment by recording global transcriptomic and metabolic responses of bacterial cultures shifted for 10 min from 37oC to a sub-lethal (43oC) or eventually lethal (48oC) temperature. A relevant metabolic model of the combined action of specific stress response mechanisms with more general, energy-regulating metabolic pathways in heat-shocked S. aureus was designed. While S. aureus cultures shifted to 43oC or left at 37oC showed marginal differences in growth and survival rates, bacterial cultures exposed to 48oC showed a rapid growth arrest followed by a subsequent decline in viable counts. The most substantial heat shock-induced changes at both 43oC and 48oC occurred in transcript levels of HrcA- and CtsR-regulated genes, encoding classical chaperones DnaK and GroESL, and some Hsp100/Clp ATPases components, respectively. Other metabolic pathways up-regulated by S. aureus exposure at 48oC included genes encoding several enzymes coping with oxidative stress, and DNA damage, or/and impaired osmotic balance. Some major components of the pentose phosphate cycle and gluconeogenesis were also up-regulated, which reflected depletion of free glucose by bacterial cultures grown in Mueller-Hinton broth prior to heat shock. In contrast, most purine- and pyrimidine-synthesis pathway components and amino acyl-tRNA synthetases were down-regulated at 48oC, as well as arginine deiminase and major fermentative pathway components, such as alcohol, lactate and formate dehydrogenases. Despite the heat-induced, increased requirements for ATP-dependent macromolecular repair mechanisms combined with declining energy sources, intracellular ATP levels remained remarkably constant during heat shock. In conclusion, the sequential loss of replication and viability at 48oC cannot be explained by significant reductions in intracellular ATP levels, but may reflect ATP rerouting for macromolecular repair mechanisms and cell survival. Our metabolic model also suggests that heat-stressed S. aureus should down-regulate the production of potential, DNA-damaging reactive oxygen species that might result from electron transport-generated ATP, involving excessive levels of free heavy metals, in particular iron. Keywords: Staphylococcus aureus; heat shock; stress responses; transcriptomic profiling; physiological adjustment Comparative transcriptomic profiling of late log phase cultures of S. aureus ISP794, exposed to 43°C vs. 37°C, or 48°C vs. 37°C. We performed triplicate measurements from independently grown cultures for each heat stress condition.
2010-06-19 | E-GEOD-12920 | biostudies-arrayexpress