FIG 1.

Model for recruitment and activation of FtsWI. FtsQLB localizes to the Z ring and recruits FtsW in a ^cytoFtsL-dependent manner with FtsW recruiting FtsI. FtsN arrives, and ^cytoFtsN interacts with FtsA in the cytoplasm, and the ^EFtsN domain acts in the periplasm, switching both FtsA and FtsQLB from the OFF to the ON conformation, resulting in activation of FtsWI. In the model, activation occurs when the AWI (activation of FtsWI) domain in FtsL (which overlaps the CCD [constriction control domain]) becomes available to contact FtsI. Activation mutations (*) in ftsA, ftsB, ftsL, and ftsW require less FtsN. FtsB* and FtsL* are thought to switch FtsQLB to the ON state. FtsA* may also do this, whereas FtsW* is likely to lead to an enzymatically active form of FtsW. For simplicity ZipA, FtsEX, and FtsK are not depicted. FtsZ, FtsA, FtsB, FtsQ, FtsL, FtsW, FtsI, and FtsN are indicated by single letters. The red rectangles highlight interactions between FtsL and FtsWI.