The ClpX chaperone controls autolytic splitting of Staphylococcus aureus daughter cells, but is bypassed by β-lactam antibiotics or inhibitors of WTA biosynthesis
Fig 8
Model of temperature dependent lysis of S. aureus clpX mutant.
At 37°C (upper panel), progression from an early (A) to a late septal ingrowth (B) occurs in the absence of ClpX activity. Upon septum closure, release of cross-linking substrates from the TP domain of PBPs in combination with teichoic acid biosynthesis serve as signals to activate autolytic splitting of daughter cells (C). At 30°C (lower panel), progression from an early to a late septal ingrowth becomes more dependent on assistance from the ClpX chaperone, and in the absence of ClpX, septum synthesis occasionally stalls in an early septal ingrowth that put the cells at risk for activation of Sle1- mediated autolytic splitting from the peripheral wall (D). Cells with premature splitting will be prone to lysis due to the risk of turgor pressure forces breaking the thin and mechanically weak cell wall at the tip of the ingrowing septum (E).