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Changes in relative transcript amounts caused by treatment of streptozotocin and floxuridine in S.aureus USA300

ABSTRACT: Changes in relative transcript amounts caused by treatment of streptozotocin and floxuridine in S.aureus USA300

PROVIDER: PRJNA408150 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6055190.fastq.gz	Fastqsanger.gz
	SRR6055191.fastq.gz	Fastqsanger.gz
	SRR6055192.fastq.gz	Fastqsanger.gz
	SRR6055184.fastq.gz	Fastqsanger.gz
	SRR6055185.fastq.gz	Fastqsanger.gz

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Changes in relative transcript amounts caused by treatment of streptozotocin and floxuridine in S.aureus USA300

Project description:Staphylococcus aureus is an important human pathogen causing skin infection and many serious diseases such as pneumonia, sepsis, and toxic shock syndrome. We identified two anti-cancer drugs, streptozotocin (STZ) and floxuridine (FU), as promising lead compounds for further optimization into effective anti-virulence drugs against S. aureus infections. To understand the molecular mechanism of the in vivo efficacy of STZ and FU, we carried out RNA-seq. S. aureus USA300 was treated with 1 ug/mL (= 3.8 uM for STZ, 4 uM for FU) for 3 h. STZ treatment altered transcription of 829 genes (382 up-regulated; 447 down-regulated) whereas FU affected the transcription of 1192 genes (580 up-regulated; 612 down-regulated). Importantly, both compounds inhibited the transcription of the other virulence-regulatory systems such as Agr, Arl, and SarA. Therefore, the results indicate that the high in vivo efficacy of STZ and FU might be due to their repression of multiple virulence regulatory systems.

2018-02-13 | GSE104069 | GEO

Staphylococcus aureus subsp. aureus USA300

Project description:Changes in relative transcript amounts caused by ∆ftsH in Staphylococcus aureus USA300

| PRJNA353307 | ENA

Changes in relative transcript amounts caused by ∆ftsH in Staphylococcus aureus USA300

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

Gene expression analysis of Staphyloccoccus aureus USA300 vs USA300 agr knockout.

Project description:The study aims to compare gene expression patterns of Staphyloccoccus aureus USA300 wild type (reference) vs USA300 agr knockout(query). The agr quorum sensing system is an important regulator of density dependent gene expression. To determine the role of agr in USA300 virulence a agr mutant was constructed and differential gene expression compared to the parental wildtype.

2011-04-08 | GSE26254 | GEO

Gene expression analysis of Staphyloccoccus aureus USA300 vs USA300 sae knockout

Project description:The study aims to compare gene expression patterns of Staphyloccoccus aureus USA300 vs USA300 sae knockout. Samples were hybridized on aminosilane coated slides with 70-mer oligos.

2011-04-08 | GSE26243 | GEO

Monitoring of protein thiol-oxidation in S.aureus USA300 under hypochlorite stress using OxICAT approach.

Project description:During infections, S. aureus has to cope with the oxidative burst of activated macrophages and neutrophils, including reactive oxygen and nitrogen species (RNS, ROS) and the strong oxidant hypochloric acid. We aimed to understand the global thiol-redox state in the major pathogen S. aureus and discover new NaOCl-sensitive proteins driven by thiol-switches. Thus, we performed a quantitative redox proteomics approach based on OxICAT and analyzed the percentages of thiol-oxidation levels in S.aureus before and after sub-lethal doses of 150 µM NaOCl stress. In parallel, we searched for protein S-bacillithiolation.

2016-12-22 | PXD004918 | Pride

Project description:S.aureus USA300 LAC Vancomycin

| PRJNA526539 | ENA

Gene expression analysis of Staphyloccoccus aureus USA300 vs USA300 sae knockout

2011-04-08 | E-GEOD-26243 | biostudies-arrayexpress

Gene expression analysis of Staphyloccoccus aureus USA300 vs USA400.

Project description:In the community and clinical settings MRSA infections are more commonly caused by a USA300 strain vs a USA400 strain. The study aims to compare gene expression patterns of Staphyloccoccus aureus USA300(reference) vs USA400(query) and to determine why USA400 is being replaced by a USA300 strain.

2011-04-08 | GSE26255 | GEO

Evolution of hypervirulence during bloodstream adaptation of CA-MRSA strain USA300

Project description:The epidemic community-acquired methicillin-resistant S. aureus (CA-MRSA) clone USA300 has recently become a leading cause of hospital-associated bloodstream infections (BSI). Leveraging this recent introduction into hospitals and the limited genetic variation across the USA300 strains, we combined microbial comparative genomics with phenotypic analyses to discover adaptive mutations. USA300 isolates from BSI were found to have independently evolved single nucleotide variants in the transcriptional regulator sarZ. sarZ inactivation lead to altered expression of virulence factors, resulting in increased lethality in a murine model of BSI. Thus, USA300 strains can optimize their fitness in hospitals through evolution of higher virulence.

2022-10-08 | GSE185544 | GEO

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