There are two basic, though not mutually exclusive, possibilities for when and where the cell sets its diameter – either during the process of cell division or during cell elongation. Despite data favoring the elongation complex (see above), there is quite a bit of innuendo that diameter control is exerted as cells divide rather than being determined during actual cell elongation.
cells grown for half a division cycle in the absence of functional PBP 2 synthesize new poles with increased diameters compared to older poles, indicating that PBP 2 helps set or maintain cell width during cell division (22
). Overexpression of FtsA inhibits E. coli
cell division, and the resulting filaments enlarge at prospective septation sites (96
). In addition, E. coli
cells are not perfectly uniform cylinders capped at either end by identical hemispherical poles; instead, one pole is often slightly larger than the other (39
), implying that width differences arise during creation of new poles.
Formstone and Errington observed that the diameter increase in an mreB
-null mutant of B. subtilis
“appeared to occur at or near new division sites, whereas the old poles retained a constant width” (30
). Similar phenomena occur when B. subtilis
cells are depleted of YlaN so that they become wider at new division sites and form tapered daughter cells (38
), and when Mbl is gradually depleted from B. subtilis
so that peptidoglycan synthesis is shifted towards developing septa (43
). Also, B. subtilis ugtP
mutants are both shorter and wider (62
). Since cell length in this mutant is controlled by expressing an FtsZ inhibitor (discussed above), FtsZ may also be responsible, directly or indirectly, for determining cell width. All these examples hint that diameter change occurs during the division cycle.
When RodZ is overproduced in C. crescentus
, the cells bulge outward at their septa and have long thin connections between daughter cells, suggesting a division defect (2
). Underscoring this relationship, RodZ colocalizes with FtsZ at the septum when division begins, after which it disperses (2
). Thus, RodZ, in addition to its interactions with MreB, may exert some of its diameter-related effects during cell division.
The best counter-example for arguing that diameter is determined during elongation rather than division is the recent observation of Takacs et al that spherical C. crescentus
cells recover wild type diameter in the absence of cell division (see above) (79
). It is, of course, possible that this is a special circumstance or, perhaps more likely, that the two systems collaborate to determine cell width.