There are difficulties with all published models that attempt to explain how rod-shaped bacteria locate their midpoint in preparation for the next cell division. Many bacteria find their middle quite accurately. This evenness of partition has been measured cytologically and is implied by the persistence of synchrony under certain circumstances. Previously, a number of models for the control of cell division have been proposed based on aspects of molecular genetics, ultrastructure measurements, or biochemical kinetics. This paper points out that none of the models in spite of their quite different natures can explain the precision of the location of the division site. Here, the ‘Central Stress Model’ is proposed which depends on the partition of wall tension between the cytoplasmic membrane (CM) and the murein layer in such a way that the CM at the centre of the rod experiences a higher stress than near the poles and that this peak stress increases through the cell cycle. The model assumes that: (i) murein is not incorporated at an established pole but is incorporated diffusely over the sidewall and intensely at sites of cell constriction; (ii) CM is synthesized over the entire cell wall; (iii) the murein and CM layers are attached non-covalently to each other, and interact physically with each other; (iv) this differential location of synthesis leads to a ‘tug-of-war’ that creates differential stresses that peak at the cell centre. Because of the fluid nature of the phospholipid bilayer there is a flux of lipid from the established poles towards the cell centre as the murein sidewall elongates. The flux from the pole lowers the tension in the CM at the ends of the sidewalls and creates a peak tension in the centre. Cells also have a discontinuity in the stresses in the murein at the junction of the curved pole with the cylindrical region of the cell wall (a doubling of the hoop stress above the axial stress). Thus in addition to the midpoint of the cell, these junctions between the polar caps and the cylindrical part of the cell wall are characterized by an abrupt change in the surface stress and we suggest that this can trigger cell division at these junctions to form a chromosome-less minicell. Two other assumptions of the model are that the cell has a membrane-associated system to sense the stress, and to trigger cell division locally when a threshold has been reached. It is suggested that there is a special two-component sensory system responding to tension in the CM. As the cell cycle progresses, and the stress in the centre of the cell exceeds some threshold, a system molecule triggers a cell division event at that site. Like other two-component systems, the sensory component of this two-component system is assumed to be distributed all over the CM. It is also assumed that when the sensory component is triggered it also causes local changes that ensure that division occurs at that site. Consequently, this model can explain why sister cells have very nearly the same size (length, volume, or biomass) and why genes that control a mechanism that senses cell size and initiates cell division have never been identified because they may not exist.


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