Staphylococcus aureus GpsB, Stk, and VraSR form a cell wall surveillance network to maintain cell envelope integrity and mediate antibiotic resistance
Antibiotic resistance is an alarming threat to public health worldwide. Specifically, drug-resistant Staphylococcus aureus remains a major contributor to global mortality. Therefore, in-depth understanding of antibiotic resistance mechanisms is urgently needed to inform alternative therapeutic strategies. We previously showed that GpsB is a critical regulator of cell wall synthesis in S. aureus.…
Staphylococcus aureus poses a significant public health concern due to antibiotic resistance. This report delves into the mechanisms of drug-resistant S. aureus, focusing on the role of three key proteins: GpsB, Stk, and VraSR. GpsB regulates cell wall synthesis in S. aureus through protein-protein interactions, but how its function is modulated remains unclear.
Previous research indicated that GpsB is phosphorylated at six distinct sites by the serine/threonine kinase Stk. This study investigates the implications of GpsB phosphorylation. Three phosphosites were identified, each individually sufficient to regulate GpsB phosphorylation, potentially affecting its interaction partners. Cells lacking the gpsB gene showed increased sensitivity to fosfomycin, which became even more pronounced when Stk was deleted.
This study elucidates the collaboration between GpsB, Stk, and the VraSR system in coordinating the demand-driven availability of cell wall precursors. The findings establish GpsB as a crucial sentinel for peptidoglycan supply chain integrity, working alongside Stk and VraSR to maintain cell envelope homeostasis and contribute to antibiotic resistance.
Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.
