A dynamic model of FtsZ abundance predicts division timing A dynamic model of FtsZ abundance predicts division timing Pulsing experiment was repeated in the presence of protease inhibitor (PI) that reduced the lag time for a given TI feedrate (f = 0.28 mmol/g/h). The TI feedrate is abbreviated as f (units: mmol glucose/g dry cell weight/h). Wild‐type lag (from Fig 2A empirical fit) is indicated by the dotted gray line.The sets of proteins that are actively degraded and division‐related intersect at FtsZ and FtsN.A schematic of how FtsZ abundance changes. FtsZ is repressed by the transcriptional factor, PdhR. PdhR is activated by Crp‐cAMP. FtsZ is also degraded primarily by the ClpXP protease complex. An approximate FtsZ threshold model poses a basal synthesis rate (α0), a feedrate‐dependent synthesis (α1f), and a degradation term (the Michaelis Menten term) to explain changes in FtsZ abundance with and without pulsing. Per the model, FtsZ would deplete via degradation during starvation, be synthesized with glucose pulsing, and engender division when its abundance reaches the threshold concentration.Analytical solution of the model (Appendix Supplemental Information) plotted against data from Fig 2A (R2 = 0.86). Lag time axis is log‐scaled. Karthik Sekar et al. Mol Syst Biol 2018;14:e8623 © as stated in the article, figure or figure legend