Toporegulation of bacterial division according to the nucleoid occlusion model.

A model for the toporegulation of division in Escherichia coli is presented in which cell constriction is initiated by the combined action of a biochemical and a structural event. It is proposed that the biochemical event of termination of DNA replication causes a transient change in the pool of deoxyribonucleotides, which serves as a localized trigger that is converted to a diffusible, cytoplasmic activator of peptidoglycan synthesis. The second event involves the segregation of the nucleoids. Evidence is presented that the nucleoid suppresses the activity of peptidoglycan synthesis in its vicinity. It is proposed that active transcription/translation around the nucleoids produces a strong but short-range inhibitor which prohibits division (nucleoid occlusion). The combined effects of the locally produced termination-activator and of the diminished occlusion as a result of nucleoid segregation, guarantee that division is normally placed between the separated nucleoids. The model can explain the pattern of division-recovery of filaments, the majority of which constrict at sites which produce polar daughter cells containing two nucleoids. In addition, the model offers an explanation for the occurrence of mini-cells under a variety of conditions.