The shape of many micro-organisms can be understood in terms of the general surface stress hypothesis that hydrostatic pressure forces newly formed wall to expand in a particular direction. What distinguishes one type of organism from another is the regions of the cell where new wall growth occurs. For several classes of organisms, the pattern of growth deduced from the shape agrees with biochemical, morphological and physiological studies. Gram-negative rods, as typified by Escherichia coli, have a morphology that may be explained in several ways by this general hypothesis.
In the present paper, the morphological, autoradiographic and biochemical data concerning E. coli are reviewed. Thirteen models are considered; there is reason to reject most of them but one model that includes two others appears more satisfactory. All the models conform to the biophysical principles that it is impossible to turn over stress-bearing peptidoglycan without shape change and that growth of the sacculus requires the introduction of new oligosaccharides and their covalent linkage before cleavage of stress-bearing bonds. The model that best accounts for the experimental data assumes that, while addition of peptidoglycan all over the cell is possible and does occur, the effective surface tension is higher (and therefore the rate of wall growth is very small) in old poles than on the sides, and very much lower at the developing division sites (where the rate of wall growth is high). It is shown that, when the hydrostatic pressure is constant throughout the cell and during a large part of the cell cycle, changes in the biochemical mechanism of wall growth which correspond to a decrease in surface tension would lead to an invagination of the stress-bearing wall. An additional mechanism may, however, be needed for final closure and for the splitting of the last few covalent bonds holding the two nascent cells together.
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