Mechanics of <i>Escherichia coli</i> cell width homeostasis and bulge dynamics from MreB and septum inhibition

<i>Escherichia coli</i> cell shape and size are governed by the mechanochemistry of the cellular components. Inhibiting either cell-wall synthesis proteins such as FtsI leads to cell elongation and bulging, while inhibiting MreB cytoskeletal polymerization results in a loss of rod-shape. Here, we quantify cell shape dynamics of <i>E. coli</i> combinatorially treated with the FtsI inhibitor cephalexin and MreB inhibitor A22 and fit a shell mechanics model to the length-width dynamics to infer the range of effective mechanical properties governing cell shape. The model based on the interplay of intracellular pressure and envelope mechanics, predicts <i>E. coli</i> cell width grows and saturates. Bulging observed in cells treated with both MreB and FtsI inhibitors, is predicted by the model to result from a lower effective bending rigidity and higher effective surface tension compared with untreated. We validate the specificity of the predicted internal pressure of ∼0.6 MPa driving bulging, when placing treated cells in a hyperosmotic environment of comparable pressure results in reversal of cell bulging. Simulations of cell width dynamics predicting threshold values of envelope bending rigidity and effective surface tension required to maintain cell shape compared with experiment validate the effective mechanical limits of cell shape maintenance.