Fig. 5: Tug-of-war model of elongasome dynamics and cell size regulation.

Models for effect of number of bound active synthesis complexes on elongasome dynamics and cell size. Active synthases complexes refer to elongasome core complexes, i.e., active RodA-bPBP pairs plus accessory proteins MreC and MreD. a Model for MreB dynamics when a single synthesis complex is bound to the MreB filament. Peptidoglycan synthesis by an active single synthesis complex (purple) drives processive MreB filament motion (teal) until the synthesis complex terminates PG synthesis and unbinds from the MreB filament, leading to pausing of the MreB filament. b Model for MreB tug-of-war dynamics, assuming that maximally two synthesis complexes can bind to the MreB filament in opposite orientations. Initially, PG synthesis by the active synthesis complex (purple) drives processive motion of the MreB filament (teal). The oppositely bound inactive synthesis complex (grey) causes drag, possibly through transient interactions with the PG. Upon successful binding of the inactive synthesis complex with the PG, the MreB filament enters a paused tug-of-war state where PG synthesis by the active synthesis complex is transiently arrested. There are two possible outcomes of tug-of-war. If the active synthesis complex wins (no reversal), PG synthesis and MreB motion is resumed in the original direction. If the inactive synthesis complex wins (reversal), that complex initiates PG synthesis and the formerly active complex terminates synthesis. This leads to reversal of MreB filament motion, with the old lagging edge of the MreB filament becoming the new leading edge. c, d Speculative model for effect of elongasome synthase concentration on cell shape. At low concentrations of active elongasome synthases, eg due to the lack of one or more essential components such as RodA in this study, there is both infrequent elongasome PG synthesis and infrequent tug-of-war. This leads to a low density of long elongasome-synthesised PG strands are inserted into the cell wall, resulting in a weaker, wider cell wall. At high concentrations of active elongasome synthases, there is both frequent elongasome PG synthesis and frequent tug-of-war. This leads to a high density of short elongasome-synthesised PG strands inserted into the cell wall, again resulting in a weaker, wider cell wall. At intermediate concentrations of active elongasome synthases, there is frequent elongasome PG synthesis but infrequent tug-of-war. This leads to a high density of long elongasome-synthesised PG strands inserted into the cell wall, resulting in a narrow, optimally strong cell wall.