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

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.

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

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.

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

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.

A lack of oxygen activates a pathway that causes the bacterial cell wall to break down, which, in turn, aids bacterial biofilm development.

Life-threatening S. aureus infections emerge from commensal nose bacteria in association with repeatable adaptive evolution.

Structural and genetic analyses reveal the highly evolved and unprecedented biological strategy used by SaPIs to spread in nature.

To avoid recognition by the immune system, bacteria use autolysins to trim fragments of peptidoglycans that are exposed on the bacterial cell wall.