During Staphylococcus aureus infections, bacterial cells bifurcate into distinct, specialized cell types that localize physically in different colonization tissues to simultaneously generate different infection types.

The absence of oxygen prompts Staphylococcus aureus cells to rupture resulting in increased formation of biofilms, which are the etiological agents of recurrent infections.

Cryo-electron microscopy and genetics show how Staphylococcus aureus pathogenicity island 1 hijacks the assembly pathway of a helper phage for its own propagation.

Neutrophil-dependent innate immune responses to the human pathogen, methicillin-resistant Staphylococcus aureus, are modulated by an interplay between interleukin-21 and type 1 interferons.

The asymptomatic colonization and importation of methicillin-resistant Staphylococcus aureus (MRSA) in hospital settings can be inferred from observed cases using combined model-inference methods and used to inform improved interventions.

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.

Morphological constraints dictate division mode in the human pathogen Staphylococcus aureus.

Genome-wide association studies have established staphylococcal pyomyositis as a disease whose pathogenesis depends critically on expression of a single toxin, Panton–Valentine leukocidin.

Inter-molecular cross-seeding between phenol-soluble modulins facilitates rapid and efficient self-assembly in Staphylococcus aureus biofilms revealing a complex molecular interplay between distinct phenol-soluble modulins orchestrating functional amyloid formation.

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.