Fig. 5. Mobilisation-and-capture of Pal by the Tol assembly drives active Pal accumulation at division sites.

The following model views the periplasm as divided into two compartments separated by a porous peptidoglycan cell wall; the ‘outer periplasm’ is close to the outer membrane while the ‘inner periplasm’ is close to the inner membrane. a Non-dividing cells. In this state, TolQ-TolR-TolA is free to diffuse in the inner membrane. Periplasmic TolB enhances Pal mobility by blocking Pal’s association with peptidoglycan, but also marks the complex for active dissociation by TolQ-TolR-TolA via the N-terminus of TolB. We propose that TolA pulls TolB through the holes that exist in the peptidoglycan layer to the inner periplasm. Thereafter, TolB diffuses back through the peptidoglycan to the outer periplasm to repeat the process. Notwithstanding this recycling, however, Pal is predominantly free of TolB in non-dividing cells and therefore bound to the peptidoglycan layer, slowing its diffusion. b Dividing cells. The TolQ-TolR-TolA complex is recruited to the divisome which localizes its TolB capturing activity. This leads to an overall lowering of the level of TolB transduction through the peptidoglycan layer and consequently greater numbers of TolB molecules in the outer periplasm and as a result greater Pal mobility throughout the cell, except at the septum. Septal Pal is kept free of TolB by localized TolQ-TolR-TolA. As TolB-Pal complexes diffuse past the septum they are actively dissociated, releasing Pal. TolB is recycled to mobilise other Pal molecules away from the septum. Hence, only in dividing cells do the small number of TolBs enhance the mobility of a much larger population of Pal molecules, TolB acting essentially as an amplifier. The end result is that more and more Pal molecules become sequestered at the divisome where they stabilize the link between the OM and the underlying cell wall in daughter cells.