The Staphylococcus aureus non-coding RNA IsrR regulates TCA cycle activity and virulence.

Staphylococcus aureus has evolved mechanisms to cope with low iron (Fe) availability in host tissues. Staphylococcus aureus uses the ferric uptake transcriptional regulator (Fur) to sense titers of cytosolic Fe. Upon Fe depletion, apo-Fur relieves transcriptional repression of genes utilized for Fe uptake.

The small non-coding RNA IsrR regulates TCA cycle activity and virulence.

has evolved mechanisms to cope with low iron (Fe) availability in host tissues. uses the ferric uptake transcriptional regulator (Fur) to sense titers of cytosolic Fe. Upon Fe depletion, apo-Fur relieves transcriptional repression of genes utilized for Fe uptake.

RNA Extraction from Gram-Positive Bacteria Membrane Vesicles Using a Polymer-Based Precipitation Method.

Investigations into the biological role and composition of bacterial extracellular vesicles have grown in popularity in recent years. Vesicles perform a variety of functions during interactions with eukaryotic host cells, ranging from antibiotic resistance to immune modulation. It is necessary to isolate vesicles in order to understand their biological functions.

The Streptococcus agalactiae Exonuclease ExoVII Is Required for Resistance to Exogenous DNA-Damaging Agents.

Streptococcus agalactiae is a human pathogen responsible for severe invasive infections in newborns. In this bacterium, XseB, a part of the ExoVII exonuclease, was shown to be specifically more abundant in the hypervirulent ST-17 strains. In Escherichia coli, ExoVII is associated either with mismatch repair or with recombinational DNA repair and is redundant with other exonucleases.

The Small Protein ScrA Influences Staphylococcus aureus Virulence-Related Processes via the SaeRS System.

Staphylococcus aureus is a Gram-positive commensal and opportunistic pathogen able to cause diseases ranging from mild skin infections to life-threatening endocarditis and toxic shock syndrome. The ability to cause such an array of diseases is due to the complex S. aureus regulatory network controlling an assortment of virulence factors, including adhesins, hemolysins, proteases, and lipases.