Moreover, in the absence of Ga5DH, some FtsZ failed to localize to the potential division sites.
These recent data indicate that the division sites are the most important places for MinCDJ action.
However, the cytokinetic ring does not disassemble and remains in close proximity to recently used division sites.
The preferential localization of B. subtilis MinC [35] and MinJ ([36], [37] and this work) to new division sites supports this role.
It also appears that the poles are actually a secondary localization site for MinC, with the protein mostly localized to active division sites.
We found that in the absence of a functional Min system, FtsA, FtsL and PBP-2B remain associated with completed division sites.
The MinE protein, which is known to prevent the division inhibitor from acting at internal division sites, was activated, whereas the minD gene, which is a cell division inhibitor, was repressed.
For the sake of clarity, recently completed division sites are denoted as new poles (a membrane stain was used to distinguish ongoing and completed septation), while other poles are referred to as old poles.
However, recently it was shown that the highest chance of minicell formation actually occurs at recently completed division sites, and not at the old poles, challenging the role of the Min system [35].
Positional control of cell division is exerted by two mechanisms: nucleoid occlusion, through Noc, which prevents division through nucleoids, and the Min system, where the combined action of the MinC, D and J proteins prevents formation of the FtsZ ring at cell poles or recently completed division sites.
Taken together, we postulate that the main function of the Min system is to prevent minicell formation adjacent to recently completed division sites by promoting the disassembly of the cytokinetic ring, thereby ensuring that cell division occurs only once per cell cycle.
