Reslane Itidal, Watson Gabrielle F, Handke Luke D, Fey Paul D
Department of Pathology, Microbiology, and Immunology, University of Nebraska Medical Center, Omaha, NE 68198, U.S.A.
Biochem Soc Trans. 2024 Dec 19;52(6):2513-2523. doi: 10.1042/BST20240710.
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.
金黄色葡萄球菌是一种极具重要性的病原体，具有多种经过充分研究和明确界定的毒力因子。然而，促进感染所需的代谢途径尚未得到充分描述。先前的数据表明，金黄色葡萄球菌在感染初期需要葡萄糖分解代谢。因此，某些生物合成途径受碳分解代谢物阻遏和CcpA调控的营养物质，包括精氨酸，必须从宿主获取。然而，尽管金黄色葡萄球菌编码了合成精氨酸的途径，但即使在没有葡萄糖的情况下，精氨酸的生物合成也受到抑制。为什么金黄色葡萄球菌是一种功能性精氨酸营养缺陷型？这篇综述讨论了最近描述的与以脯氨酸或谷氨酸为底物抑制精氨酸生物合成相关的调控机制。此外，还讨论了最近的研究，这些研究深入了解了将精氨酸营养缺陷型与感染持续存在联系起来的最终机制。
