Mechanics ofE. colicell width homeostasis and bulging dynamics from MreB and septum inhibition

Abstract

The mechanobiology of cytoskeleton and cell envelope play a vital role in cell shape homeostasis. In the gram-negative model rod-shaped bacterium Escherichia coli antibiotics that weaken the cell envelope are seen to result in bulges that eventually lead to lysis. Here, we quantify the shape dynamics of E. coli treated with cephalexin, a PBP3 inhibitor and A22, an MreB polymerization inhibitor from single cell microscopy. We find low concentrations of both inhibitors result in bulge formation with multiple cell shapes observed: rugby, large bacilli and rods with two and three bulges. We quantify the parameters of cell envelope rigidity, pressure and fluidity obtained from fitting a computational model of shell-mechanics to length and width dynamics from experiment. Using this optimized model we estimate the turgor and growth pressures of untreated growing cells as approx. 0.15 MPa and approx. 0.4 MPa. The bulge expansion dynamics correlate most prominently with a change in bending rigidity of the cell wall and cytoskeleton. Simulations predict a threshold behavior in response to envelope bending rigidity that is validated by comparison with experiments of E. coli treated with A22 either in isolation or in combination, resulting in loss of width control and cell shape change.