Application of Two-Dimensional Difference Gel Electrophoresis in Identification of Factors Responsible for Virulence of Staphylococcus aureus

Bonar, Emilia; Chlebicka, Kinga; Dubin, Grzegorz; Władyka, Benedykt

doi:10.1007/978-1-4939-9849-4_11

Cited by 1 publication

(1 citation statement)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Sample preparation and 2D DIGE (two-dimensional difference gel electrophoresis) proteomic analysis were performed as described in [ 19 ]. Briefly, for cellular protein isolation, bacteria from the logarithmic and the stationary phase of growth (3.5 h and 15 h post-inoculation, respectively) were pelleted by centrifugation (5 min, 5000× g , 4 °C), washed twice with phosphate buffer saline, and suspended in TRI-Reagent (Sigma, Darmstadt, Germany).…”

Section: Methodsmentioning

confidence: 99%

Impacts of the Type I Toxin–Antitoxin System, SprG1/SprF1, on Staphylococcus aureus Gene Expression

Chlebicka

Bonar

Suder

et al. 2021

Genes

Self Cite

View full text Add to dashboard Cite

Type I toxin–antitoxin (TA) systems are widespread genetic modules in bacterial genomes. They express toxic peptides whose overexpression leads to growth arrest or cell death, whereas antitoxins regulate the expression of toxins, acting as labile antisense RNAs. The Staphylococcus aureus (S. aureus) genome contains and expresses several functional type I TA systems, but their biological functions remain unclear. Here, we addressed and challenged experimentally, by proteomics, if the type I TA system, the SprG1/SprF1 pair, influences the overall gene expression in S. aureus. Deleted and complemented S. aureus strains were analyzed for their proteomes, both intracellular and extracellular, during growth. Comparison of intracellular proteomes among the strains points to the SprF1 antitoxin as moderately downregulating protein expression. In the strain naturally expressing the SprG1 toxin, cytoplasmic proteins are excreted into the medium, but this is not due to unspecific cell leakages. Such a toxin-driven release of the cytoplasmic proteins may modulate the host inflammatory response that, in turn, could amplify the S. aureus infection spread.

show abstract

Section: Methodsmentioning

confidence: 99%