Document Type

Article

Publication Date

12-10-2024

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.

Comments

The pdf passed the Adobe accessibility checker prior to upload.

This article was published open access under the Cambridge University Press and University of Nebraska at Omaha open access publishing agreement.

Download

Files over 3MB may be slow to open. For best results, right-click and select "save as..."

Share

COinS