Impact of the Histidine‐Containing Phosphocarrier Protein HPr on Carbon Metabolism and Virulence in Staphylococcus aureus

Authors

Linda Pätzold, Saarland UniversityFollow
Anne-Christine Brausch, Saarland University
Evelyn-Laura Bielefeld, Saarland UniversityFollow
Lisa Zimmer, Saarland UniversityFollow
Greg A. Somerville, University of NebraskaFollow
Markus Bischoff, University of SaarlandFollow
Rosmarie Gaupp, Saarland UniversityFollow

Document Type

Article

Date of this Version

2021

Citation

Pätzold, L.; Brausch, A.‐C.; Bielefeld, E.‐L.; Zimmer, L.; Somerville, G.A.; Bischoff, M.; Gaupp, R. Impact of the Histidine‐ Containing Phosphocarrier Protein HPr on Carbon Metabolism and Virulence in Staphylococcus aureus. Microorganisms 2021, 9, 466. https://doi.org/10.3390/microorganis ms9030466

Comments

2021 by the authors.

Abstract

Carbon catabolite repression (CCR) is a common mechanism pathogenic bacteria use to link central metabolism with virulence factor synthesis. In gram‐positive bacteria, catabolite control protein A (CcpA) and the histidine‐containing phosphocarrier protein HPr (encoded by ptsH) are the predominant mediators of CCR. In addition to modulating CcpA activity, HPr is essential for glucose import via the phosphotransferase system. While the regulatory functions of CcpA in Staphylococcus aureus are largely known, little is known about the function of HPr in CCR and infectivity. To address this knowledge gap, ptsH mutants were created in S. aureus that either lack the open reading frame or harbor a ptsH variant carrying a thymidine to guanosine mutation at position 136, and the effects of these mutations on growth and metabolism were assessed. Inactivation of ptsH altered bacterial physiology and decreased the ability of S. aureus to form a biofilm and cause infections in mice. These data demonstrate that HPr affects central metabolism and virulence in S. aureus independent of its influence on CcpA regulation.