Conclusions

E. coli cells possessing cfc mutations divide before they reach the size at which cfc+ cells divide, and produce many small cells–each with a single nucleoid. The mutations affect the timing of cell division, but not the initiation mass for chromosome replication. This is because of a reduction in the length of the period between nuclear division and cell division, and a compensatory increase in the time interval between cell division and initiation of the next round of DNA replication. These mutations relieve cells from division arrest caused by the inhibition of DNA replication. As such, the cfc mutants are defective in a signaling mechanism that couples DNA replication and cell division. I conclude that Ap4A is part of this signaling mechanism.