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Prophage-encoded methyltransferase upregulates virulence to drive adaptation in an outbreak of community-acquired methicillin-resistant Staphylococcus aureus [Harm analysis]

ABSTRACT: Prophage-encoded methyltransferase upregulates virulence to drive adaptation in an outbreak of community-acquired methicillin-resistant Staphylococcus aureus [Harm analysis]

PROVIDER: PRJNA1074732 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27918977_1.fastq.gz	Fastqsanger.gz
	SRR27918977_2.fastq.gz	Fastqsanger.gz
	SRR27918978_1.fastq.gz	Fastqsanger.gz
	SRR27918978_2.fastq.gz	Fastqsanger.gz
	SRR27918979_1.fastq.gz	Fastqsanger.gz

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Prophage-encoded methyltransferase upregulates virulence to drive adaptation in an outbreak of community-acquired methicillin-resistant Staphylococcus aureus

Project description:Prophage-encoded methyltransferase upregulates virulence to drive adaptation in an outbreak of community-acquired methicillin-resistant Staphylococcus aureus

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Prophage-encoded methyltransferase upregulates virulence to drive adaptation in an outbreak of community-acquired methicillin-resistant Staphylococcus aureus

Project description:To determine the effects of phage adenine methyltransferase (pamA) on gene expression in WT USA300 (LAC*)

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Prophage-encoded methyltransferase upregulates virulence to drive adaptation in an outbreak of community-acquired methicillin-resistant Staphylococcus aureus [Harm analysis]

Project description:To determine the effects of phage m⏀11 on gene expression in USA300 (LAC*)

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Therapeutic SHPRH-146aa encoded by circ-SHPRH dynamically upregulates P21 to inhibit CDKs in neuroblastoma

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Toxin mediates sepsis caused by methicillin-resistant Staphylococcus epidermidis

Project description:Bacterial sepsis is a major killer in hospitalized patients. Coagulase-negative staphylococci (CNS) with the leading species Staphylococcus epidermidis are the most frequent causes of nosocomial sepsis, with most infectious isolates being methicillin resistant. However, which bacterial factors underlie the pathogenesis of CNS sepsis is unknown. While it has been commonly believed that invariant structures on the surface of CNS trigger sepsis by causing an over-reaction of the immune system, we show here that sepsis caused my methicillin-resistant S. epidermidis is to a large extent mediated by the methicillin resistance island-encoded peptide toxin, PSM-mec. PSM-mec contributed to bacterial survival in whole human blood and resistance to neutrophil-mediated killing, and caused significantly increased mortality and cytokine expression in a mouse sepsis model. Furthermore, we show that the PSM-mec peptide itself, rather than the regulatory RNA in which its gene is embedded, is responsible for the observed virulence phenotype. While toxins have never been clearly indicated in CNS infections, our study shows that an important type of infection caused by the predominant CNS species, S. epidermidis, is mediated to a large extent by a toxin. Of note, these findings suggest that CNS infections may be amenable to virulence-targeted drug development approaches. We used microarrays to detail the global gene expression between S. epidermidis strain Rp62A and S. epidermidis strain Rp62A isogenic Δpsm-mec deletion mutants

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Project description:Prophage-encoded methyltransferase drives adaptation of community-acquired methicillin-resistant Staphylococcus aureus

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Project description:We used RNA-seq to conduct a genome-wide transcriptomic analysis of the C. difficile strain R20291 carrying the newly introduced ϕCD38-2 prophage. A total of 39 bacterial genes were differentially expressed in the R20291 lysogen, 26 of them being downregulated. Several of the regulated genes encode transcriptional regulators and PTS subunits involved in glucose, fructose and glucitol/sorbitol uptake and metabolism. Also of note, the presence of ϕCD38-2 upregulated the expression of a group of regulatory genes located in phi-027, a resident prophage common to most ribotype 027 isolates. The most differentially expressed gene was the conserved phase-variable cell wall protein CwpV, which was upregulated by about 20-fold in the lysogen. This is the first study describing the global response of C. difficile to the presence of a newly introduced prophage.

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