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Gene expression analysis of Vancomycin resistance in Stapyloccoccus aureus strains: 2275, 2279, 2276, 2277, 2278, and 2283.

ABSTRACT: 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.

ORGANISM(S): Staphylococcus aureus

PROVIDER: GSE26353 | GEO | 2011/04/08

SECONDARY ACCESSION(S): PRJNA136735

REPOSITORIES: GEO

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Gene expression analysis of Vancomycin resistance in Stapyloccoccus aureus strains: 2275, 2279, 2276, 2277, 2278, and 2283.

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

Gene expression analysis of Vancomycin resistance in Stapyloccoccus aureus strains: PA, C1 and T8.

2011-04-08 | GSE26400 | GEO

A mutation in PP2C Phosphatase Gene in a Staphylococcus aureus USA300 Clinical Isolate with Reduced Susceptibility to Vancomycin and Daptomycin

2012-08-03 | GSE39868 | GEO

A mutation in PP2C Phosphatase Gene in a Staphylococcus aureus USA300 Clinical Isolate with Reduced Susceptibility to Vancomycin and Daptomycin

Project description:Investigation of baseline transcription activity of two different clinical isolates of Staphylococcus aureus with two different susceptibility levels to the antibiotics Vancomycin and Daptomycin. Two different strains of Staphylococcus aureus, one that is fully Vancomycin and Daptomycin Sensitive and one with decreased Vancomycin and Daptomycin Sensitivity - grown to mid-log phase in rich broth.

2012-08-03 | E-GEOD-39868 | biostudies-arrayexpress

Switching on antibiotic resistance in Staphylococcus aureus – Contribution of WalK and VraS histidine kinases in the development of vancomycin and daptomycin resistance

Project description:Staphylococcus aureus is a notorious bacterial pathogen that causes a broad range of human diseases, and isolates that are resistant to several antibiotic classes including last resort antibiotics like vancomycin and daptomycin complicate the situation. We characterized S. aureus VC40, a strain that shows full resistance to vancomycin (MIC of 64 µg/ml) and daptomycin (MIC of 4 µg/ml) as well as a decreased susceptibility to further cell wall active agents. Genome sequencing revealed mutations in genes encoding the histidine kinases WalK and VraS that control cell envelope related processes and gene expression profiling indicated the induction of the respective regulons in strain VC40. Reconstitution of the mutations in walK or vraS into the susceptible S. aureus NCTC 8325 background resulted in a considerably increased resistance to vancomycin and daptomycin with MICs surpassing the clinical breakpoints for these antibiotics, thereby generating vancomycin-intermediate S. aureus (VISA) strains. As observed for S. aureus VC40, the walKwalk and vraS mutations also led to an increased expression of the respective regulons in the NCTC 8325 background. Phenotypic studies showed that S. aureus VC40 as well as the walKwalk and vraS mutants of strain NCTC 8325 were characterized by a significantly thickened cell wall, a decreased growth rate, a reduced autolytic activity and an increased resistance to lysostaphin-induced lysis. These results demonstrate that the WalK and VraS histidine kinases act as major switches which allow S. aureus to rapidly develop vancomycin resistance up to the VISA level via mutation of one single gene locus and concomitantly contribute to cross-resistance to other antibiotics including the last resort antibiotic daptomycin.

2014-08-18 | GSE46887 | GEO

Switching on antibiotic resistance in Staphylococcus aureus M-bM-^@M-^S Contribution of WalK and VraS histidine kinases in the development of vancomycin and daptomycin resistance

Project description:Staphylococcus aureus is a notorious bacterial pathogen that causes a broad range of human diseases, and isolates that are resistant to several antibiotic classes including last resort antibiotics like vancomycin and daptomycin complicate the situation. We characterized S. aureus VC40, a strain that shows full resistance to vancomycin (MIC of 64 M-BM-5g/ml) and daptomycin (MIC of 4 M-BM-5g/ml) as well as a decreased susceptibility to further cell wall active agents. Genome sequencing revealed mutations in genes encoding the histidine kinases WalK and VraS that control cell envelope related processes and gene expression profiling indicated the induction of the respective regulons in strain VC40. Reconstitution of the mutations in walK or vraS into the susceptible S. aureus NCTC 8325 background resulted in a considerably increased resistance to vancomycin and daptomycin with MICs surpassing the clinical breakpoints for these antibiotics, thereby generating vancomycin-intermediate S. aureus (VISA) strains. As observed for S. aureus VC40, the walKwalk and vraS mutations also led to an increased expression of the respective regulons in the NCTC 8325 background. Phenotypic studies showed that S. aureus VC40 as well as the walKwalk and vraS mutants of strain NCTC 8325 were characterized by a significantly thickened cell wall, a decreased growth rate, a reduced autolytic activity and an increased resistance to lysostaphin-induced lysis. These results demonstrate that the WalK and VraS histidine kinases act as major switches which allow S. aureus to rapidly develop vancomycin resistance up to the VISA level via mutation of one single gene locus and concomitantly contribute to cross-resistance to other antibiotics including the last resort antibiotic daptomycin. Microarray was used to evaluate alteration in the transcriptome of mutS mutant and compared to the parental strain VC40

2014-08-18 | E-GEOD-46887 | biostudies-arrayexpress

Gene expression analysis of Vancomycin resistance in Stapyloccoccus aureus strains: PA, C1 and T8.

Project description:The study aims to identify genes associated with Vancomycin resistance. Wild type and a mutant cells line were treated with antibiotic at multiple concentrations and RNA samples extracted over a two hour time course.Staphylococcus aureus strain PA is the reference for this series. Wild type and a mutant cells line were treated with antibiotic at multiple concentrations and RNA samples extracted over a two hour time course. Samples were hybridized on aminosilane coated slides with 70-mer oligos.

2011-04-08 | E-GEOD-26400 | biostudies-arrayexpress

Cervimycin resistant Staphylococcus aureus strains display a vancomycin intermediate resistant phenotype

Project description:Resistance to antibiotics is an emerging problem and necessitates novel antibacterial therapies. Cervimycins A‒D are natural products of Streptomyces tendae HKI 0179 with promising activity against multidrug resistant staphylococci and vancomycin resistant enterococci. We studied the mode of action of cervimycin C and D by selection of cervimycin resistant (CmR) Staphylococcus aureus strains. Genome sequencing of CmR mutants revealed amino acid exchanges in the essential histidine kinase WalK, the Clp protease proteolytic subunit ClpP or the Clp ATPase ClpC, and the heat shock protein DnaK. Interestingly, all characterized cervimycin resistant mutants harbored a combination of mutations in walK and clpP or clpC. Mutations in the Clp system abolished ClpP or ClpC activity, and the deletion of clpP rendered S. aureus but not B. subtilis cervimycin resistant. The essential gene walK was the second mutational hotspot in the cervimycin resistant S. aureus mutants, which decreased WalK activity in vitro and generated a vancomycin intermediately resistant phenotype, with a thickened cell wall, a slower growth rate, and reduced cell lysis. Transcriptomic and proteomic analysis revealed massive alterations in the CmR strains , with major alterations in the heat shock regulon, the metal ion homeostasis and the carbohydrate metabolism. Taken together, compensatory mutations in cervimycin resistant mutants induced a VISA phenotype in S. aureus, suggesting cell wall metabolism or the ClpCP proteolytic system as primary target of the polyketide antibiotic

2022-09-08 | GSE206309 | GEO

RNase III-CLASH of multi-drug resistant Staphylococcus aureus reveals a regulatory mRNA 3’UTR required for intermediate vancomycin resistance

Project description:Treatment of methicillin-resistant Staphylococcus aureus (MRSA) infections is dependant on the efficacy of last-line antibiotics like vancomycin. Vancomycin treatment failure is most commonly linked to the emergence of vancomycin-intermediate resistance in clincal isolates (termed VISA). These isolates have not acquired resistance genes but appear to accumulate a heterogenous collection of single nucleotide polymerisms that collectively alter the physiology of the cell to increase vancomycin tolerance. Cell wall thickening is common among VISA isolates and is thought to decrease vancomycin permeability. Changes in regulatory sRNA expression have been correlated with antibiotic stress responses in VISA isolates however the functions of the vast majority of these RNA regulators is unknown. Here we have used the endoribonuclease RNase III to capture RNA-RNA interactions using an RNA proximity-dependant ligation technique termed CLASH. RNase III-CLASH uncovered hundreds of sRNA-mRNA interactions in vivo allowing functional characterisation of many sRNAs for the first time. Surprisingly, we find that an mRNA encoding an unusually long 3’UTR (here termed vigR) functions as a regulatory ‘hub’ within our RNA-RNA interaction network. We demonstrate vigR promotes expression of the cell wall lytic transglycosylase encoded by isaA through a direct mRNA-mRNA interaction. Further, we find that the vigR mRNA 3’UTR is required for cell wall thickening and that deletion of the vigR 3’UTR re-sensitises VISA to vancomycin. Our results demonstrate the utility of RNase III-CLASH for identifying new regulatory RNA functions and indicate that S. aureus may use mRNA-mRNA interactions to co-ordinate gene expression much more widely than previously appreciated.

2021-09-14 | GSE158830 | GEO

Effect of Hamamelitannin, vancomycin and combination treatment of Hamamelitannin and vancomycin on gene expression in S. aureus Mu50 biofilms

Project description:Novel anti-infective agents targeting Staphylococcus aureus and capable of increasing S. aureus susceptibility towards antibiotics are needed. One alternative approach is targeting the bacterial quorum sensing (QS) system. QS is a process by which bacteria produce and detect signal molecules and thereby coordinate their behaviour, virulence and biofilm formation in a cell-density-dependent manner. Hamamelitannin (HAM) was previously suggested to target the S. aureus QS system, thereby increasing the susceptibility of S. aureus biofilms towards vancomycin. However, mechanistic insights are still lacking. For this reason, we evaluated the effect of Hamamelitannin, vancomycin and combination treatment of Hamamelitannin and vancomycin on gene expression in S. aureus Mu50 biofilms.

2017-08-25 | E-MTAB-3816 | biostudies-arrayexpress

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