Regulatory dynamics of arginine metabolism in Staphylococcus aureus

Abstract

Staphylococcus aureus is a highly significant pathogen with several well studied and defined virulence factors. However, the metabolic pathways that are required to facilitate infection are not well described. Previous data have documented that S. aureus requires glucose catabolism during initial stages of infection. Therefore, certain nutrients whose biosynthetic pathway is under carbon catabolite repression and CcpA, including arginine, must be acquired from the host. However, even though S. aureus encodes pathways to synthesize arginine, biosynthesis of arginine is repressed even in the absence of glucose. Why is S. aureus a functional arginine auxotroph? This review discusses recently described regulatory mechanisms that are linked to repression of arginine biosynthesis using either proline or glutamate as substrates. In addition, recent studies are discussed that shed insight into the ultimate mechanisms linking arginine auxotrophy and infection persistence.