The ATP-Dependent Protease ClpP Inhibits Biofilm Formation by Regulating Agr and Cell Wall Hydrolase Sle1 in Staphylococcus aureus

Frontiers in Cellular and Infection Microbiology

Xiaowei Ma¹  Lei He¹  Juanxiu Qin¹  Min Li¹  Qian Liu¹  Xing Wang²  Taeok Bae³  Won-Sik Yeo³  Sen Cheng⁴  Xiaoyun Liu⁴ 

[1] Department of Laboratory Medicine, School of Medicine, Ren Ji Hospital, Shanghai Jiao Tong UniversityShanghai, China;Department of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiao Tong UniversityShanghai, China;Department of Microbiology and Immunology, Indiana University School of Medicine-NorthwestGary, IN, USA;Institute of Analytical Chemistry and Synthetic and Functional Biomolecules Center, College of Chemistry and Molecular Engineering, Peking UniversityBeijing, China;

关键词: Staphylococcus aureus;    biofilm;    proteolysis system;    Agr;    cell wall hydrolysis;   

DOI  :  10.3389/fcimb.2017.00181

来源: DOAJ

【 摘 要 】

Biofilm causes hospital-associated infections on indwelling medical devices. In Staphylococcus aureus, Biofilm formation is controlled by intricately coordinated network of regulating systems, of which the ATP-dependent protease ClpP shows an inhibitory effect. Here, we demonstrate that the inhibitory effect of ClpP on biofilm formation is through Agr and the cell wall hydrolase Sle1. Biofilm formed by clpP mutant consists of proteins and extracellular DNA (eDNA). The increase of the protein was, at least in part, due to the reduced protease activity of the mutant, which was caused by the decreased activity of agr. On the other hand, the increase of eDNA was due to increased cell lysis caused by the higher level of Sle1. Indeed, as compared with wild type, the clpP mutant excreted an increased level of eDNA, and showed higher sensitivity to Triton-induced autolysis. The deletion of sle1 in the clpP mutant decreased the biofilm formation, the level of eDNA, and the Triton-induced autolysis to wild-type levels. Despite the increased biofilm formation capability, however, the clpP mutant showed significantly reduced virulence in a murine model of subcutaneous foreign body infection, indicating that the increased biofilm formation capability cannot compensate for the intrinsic functions of ClpP during infection.

【 授权许可】

Unknown