Figure 5.

The progression permission model can accommodate diverse situations. (A) Perturbations of chromosome/divisome events that delay PCC formation. (B) Growth rate transitions. It is well established that, in a given growth condition, replication initiation tends to occur at a particular cell mass (sometimes parameterized as the mass/origin ratio; Donachie, 1968). Thus, in some situations, a change in growth conditions can be implemented by the simple expedient of having replication initiation occur at the cell mass corresponding to the new growth rate (B). However, some situations, notably a dramatic increase in growth rate, require that replication initiate before the time at which it would normally be allowed to occur by a scheduled progression permission event. In such cases, the required adjustment can be made if PCC activity is compromised in such a way that it still forms in response to onset of a (C+D) sequence, and regulates the ensuing division, but is no longer able to regulate replication initiation. As a result, initiation can run free until such time as a properly constituted PCC has again formed (C). Open hexagon indicates the (C+D) period in which PCC control over replication intiation is abrogated. Orange circles denote the replication initiations that are determined independently of PCC control due to the combined effects of PCC control abrogation and timing relative to re-establishment of PCC control. This scenario corresponds to the Cooper-Helmstetter observations that ongoing C period(s) is/are completed before there is a change to a new interval between divisions [the phenomenon of “rate maintenance” Helmstetter et al., 1968]; compare orange and turquoise double-headed arrows in (B,C).