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The Center and Right Insets zoom in on regions missing a single peptide or glycan, respectively, shown as broken blue links.

S1 and Materials and Methods for more details). ( A) The Left Inset zooms in on a region of the cell wall without defects and schematically illustrates the elastic forces on each vertex (see Fig. Both are under tension due to osmotic pressure. Glycan strands (shown in green) are hoops that wrap around the circumference of the cylinder, whereas peptide crosslinks (shown in red) are longitudinal. Finally, we show that many common bacterial cell shapes can be realized within the same model via simple spatial patterning of peptidoglycan defects, suggesting that minor patterning changes could underlie the great diversity of shapes observed in the bacterial kingdom.Įlastic model of the peptidoglycan network predicts “cracked” cell shapes. Our physical model also suggests a surprising robustness of cell shape to peptidoglycan defects, helping explain the observed porosity of the cell wall and the ability of cells to grow and maintain their shape even under conditions that limit peptide crosslinking. To test these predictions, we use time-lapse imaging experiments to show that damage often manifests as a bulge on the sidewall, coupled to large-scale bending of the cylindrical cell wall around the bulge. In this work, we introduce a quantitative physical model of the bacterial cell wall that predicts the mechanical response of cell shape to peptidoglycan damage and perturbation in the rod-shaped Gram-negative bacterium Escherichia coli. Although many molecular details of the composition and assembly of cell-wall components are known, how the network of peptidoglycan subunits is organized to give the cell shape during normal growth and how it is reorganized in response to damage or environmental forces have been relatively unexplored. In bacterial cells, the peptidoglycan cell wall is the stress-bearing structure that dictates cell shape.