Figure 3.

Model of LapC-mediated control of LpxC degradation as a function of the demand for LPS synthesis. (a) Under normal-growth conditions, LpxC and FabZ activity is coupled, maintaining a balanced synthesis of LPS vs. phospholipids. (b) When the demand for LPS synthesis is high, such as under fast-growing conditions, LapC inhibits and traps LapB preventing the LapB–FtsH complex formation and hence preventing excessive degradation of LpxC. (c) When the LapC periplasmic domain is absent, the LapB–FtsH complex is hyperactive, leading to increased degradation of LpxC. Similarly, when the demand for LPS is less, such as under slow-growth conditions or in the stationary phase, LPS accumulates in the periplasm, leading to increased destabilization of LpxC, with LapC not inhibiting LapB effectively.