1. Impact of the Histidine-Containing Phosphocarrier Protein HPr on Carbon Metabolism and Virulence in Staphylococcus aureus
- Author
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Lisa Zimmer, Greg A. Somerville, Markus Bischoff, Rosmarie Gaupp, Anne-Christine Brausch, Evelyn-Laura Bielefeld, and Linda Pätzold
- Subjects
Microbiology (medical) ,Staphylococcus aureus ,Catabolite repression ,Virulence ,medicine.disease_cause ,Microbiology ,Virulence factor ,Article ,03 medical and health sciences ,chemistry.chemical_compound ,Virology ,Glucose import ,medicine ,lcsh:QH301-705.5 ,030304 developmental biology ,0303 health sciences ,biology ,030306 microbiology ,Chemistry ,HPr ,PEP group translocation ,CcpA ,biology.organism_classification ,carbon catabolite repression ,carbohydrates (lipids) ,lcsh:Biology (General) ,CCPA ,physiology ,bacteria ,metabolism ,Bacteria - 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.
- Published
- 2021