果冻影院

Abstract:听Evolutionarily divergent bacteria share a common phenomenological strategy for cell-size homeostasis under steady-state conditions. In the presence of inherent physiological stochasticity, cells following this recently (re)discovered 鈥渁dder鈥� principle gradually return to their steady-state size by adding a constant volume between birth and division regardless of their size at birth. However, the mechanism of the adder has been unknown despite intense efforts. Based on our new data and modeling, I will explain that the adder is a direct consequence of two general processes in biology: (1) threshold -- accumulation of initiators and precursors required for cell division to a respective fixed number, and (2) balanced biosynthesis -- maintenance of their production proportional to volume growth. This mechanism is naturally robust to static growth inhibition, but also allows us to 鈥渞eprogram鈥� cell-size homeostasis in a quantitatively predictive manner in both Gram-negative听Escherichia coli听and Gram-positive听Bacillus subtilis. By generating dynamic oscillations in the concentration of the division protein FtsZ, we were able to oscillate cell size at division and systematically break the adder. In contrast, periodic induction of replication initiator protein DnaA caused oscillations in cell size at initiation, but did not alter division size or the adder. Finally, we were able to restore the adder phenotype in slow growing听E. coli, the only known steady-state growth condition wherein听E. coli听significantly deviates from the adder, by repressing active degradation of division proteins. Together these results show that division and replication are independently controlled, and that division processes exclusively drive cell-size homeostasis in bacteria.