Proposed mechanism of ArlRS–MgrA cascade controlling clumping and adhesion in <i>S</i>. <i>aureus</i>.

With functional ArlRS–MgrA cascade, giant surface proteins (Ebh, SraP, SasG) are repressed, and conventional surface adhesins can mediate clumping (by crosslinking cells through fibrinogen, Fg), and adhesion of S. aureus to ligands on the vessel wall (A). Inactivation of the ArlRS–MgrA cascade leads to de-repression of Ebh, SraP and SasG, and their appearance on S. aureus cell surface prevents neighboring adhesins from interacting with their ligands, what leads to lack of clumping and adhesion (B).