Staphylococcus aureus is an important bacterial pathogen which is a leading cause of biofilm-associated infections on indwelling medical devices. Biofilms are currently estimated to be involved in more than 65 % of hospital-acquired infections. There is evidence that bacterial adhesion and biofilm formation are favored under high physical stress, but how this is achieved at the molecular level is not known. In a study published in PNAS, a LIBST team, together with the Trinity College Dublin, has elucidated the mechanism by which S. aureus responds to mechanical tension. They focused on the bacterial surface protein ClfA, and on its interaction with fibrinogen, a blood protein that rapidly covers implanted medical devices. Using atomic force microscopy, they showed that ClfA behaves as a force-sensitive molecular switch that potentiates staphylococcal adhesion under mechanical stress. The adhesion of ClfA is weak at low tensile force, but is dramatically enhanced by mechanical tension, as observed with catch bonds. Strong bonds are inhibited by a peptide mimicking Fg, which offers prospects for the development of antiadhesion therapeutics. These findings are of biological significance because they explain at the molecular level the ability of ClfA to promote bacterial attachment under high physiological shear stress. This study emphasizes the role of mechanobiology in staphylococcal biofilms, a topic that the team also discusses in a recent perspective article in Science.