FIG 1.

Schematic representation of the possible interactions and activation in the divisome. Panel A shows the divisome when FtsN is initially recruited by FtsA (31). For the model, only the relevant divisome proteins are shown. This switches FtsA to the on state, and further accumulation of FtsN allows successful competition with FtsBLQ for the peptidoglycan synthetic complex shown in panel B. FtsN activates PBP1B, which becomes hyperactive due to the absence of CpoB. The concomitant abolishment of PBP3 inhibition allows FtsW activity and the initiation of septal PG synthesis. Since none of the PG hydrolases are included in the model, at this time, we assume that the regulation of septation will be more complex than shown here.