Abstract
Escherichia coli normally divides at its equator between segregated nucleoids. Such division is inhibited during perturbations of chromosome replication (even in the absence of inducible division inhibitors); eventually, division resumes at sites which are not at this equator. Escherichia coli will also divide at its poles to generate minicells following overproduction of the FtsZ or MinE proteins. The mechanisms underlying the division inhibition and the positioning of the division sites are unknown. In the membrane tectonics model, I propose that the formation of phospholipid domains within the cytoplasmic membrane positions division sites. The particular phospholipid composition of a domain attracts particular proteins and determines their activity; conversely, particular proteins change the composition of domains. Principally via such proteins, the interaction of the chromosome with the membrane creates a chromosomal domain. The development of chromosomal domains during replication and nucleoid formation contributes to the formation and positioning of a septal domain between them. During septation (cell division), this septal domain matures into a polar domain. Each domain attracts and activates different enzymes. The septal domain attracts and activates enzymes necessary for septation. Preventing the formation of the septal domain by preventing chromosome replication prevents normal division. Altering the composition of the polar domain may allow septation enzymes to function there and generate minicells. A corollary of the model explains how the formation of an origin domain by the attachment of hemi-methylated origin DNA to the membrane may underlie the creation and migration of structures within the envelope, the periseptal annuli.
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