Robust NMR approach allowed simultaneous detection of substrate cleavage site and real-time kinetics of hydrolysis for Staphylococcus aureus peptidoglycan hydrolases lysostaphin and LytM, and revealed D-alanyl-glycine activity for LytM.

The transition of Staphylococcus aureus from commensalism to invasive disease, bacteraemia, is a complex balancing act offsetting offensive and defensive virulence strategies involving the Tca cell wall stress stimulon locus.

This time-shortened work flow improves sensitivity and specificity for the identification of bacteria in bone infections independently of bacterial culturability.

Surface protein precursors traffic to lipoteichoic acid-rich septal membranes of Staphylococcus aureus for cleavage of their YSIRK-GXXS motif signal peptides and SecA-mediated translocation across the plasma membrane.

Staphylococcus aureus NAD kinase promotes infection by protecting bacteria from host antimicrobial defenses and by supporting production of major virulence factors.

Cells must acquire multiple viral spacer sequences to neutralize mutant escaper phages and form colonies during the CRISPR-Cas immune response.

Staphylococcus aureus switches from innocuous coloniser to invasive human pathogen, the bacterial population can accumulate pathoadaptive mutations that reduce bacterial toxicity whilst allowing persistence within infected cells, potentially leading to severe human infections.

Blocking the bacterial lipid flippase MprF by monoclonal antibodies enhance staphylococcal clearance by host defense and antibiotics providing a novel proof of concept for antivirulence approaches targeting bacterial resistance mechanisms.

GpsB in Staphylococcus aureus directly regulates the central cell division protein FtsZ, a different function from that assigned for GpsB in other closely related organisms.