Bacillus subtilis MinC destabilizes FtsZ-rings at new cell poles and contributes to the timing of cell division.

Division site selection in rod-shaped bacteria depends on nucleoid occlusion, which prevents division over the chromosome and MinCD, which prevent division at the poles. MinD is thought to localize MinC to the cell poles where it prevents FtsZ assembly. Time-lapse microscopy demonstrates that in Bacillus subtilis transient polar FtsZ rings assemble adjacent to recently completed septa and that in minCD strains these persist and are used for division, producing a minicell. This suggests that MinC acts when division proteins are released from newly completed septa to prevent their immediate reassembly at new cell poles. The minCD mutant appears to uncouple FtsZ ring assembly from cell division and thus shows a variable interdivisional time and a rapid loss of cell cycle synchrony. Functional MinC-GFP expressed from the chromosome minCD locus is dynamic. It is recruited to active division sites before septal biogenesis, rotates around the septum, and moves away from completed septa. Thus high concentrations of MinC are found primarily at the septum and, more transiently, at the new cell pole. DivIVA and MinD recruit MinC to division sites, rather than mediating the stable polar localization previously thought to restrict MinC activity to the pole. Together, our results suggest that B. subtilis MinC does not inhibit FtsZ assembly at the cell poles, but rather prevents polar FtsZ rings adjacent to new cell poles from supporting cell division.