Molecular biologists have learned a great deal about the replication process by studying mutants with blocks in specific steps in replication. E.coli and the proteins that they encode along with some information about the proteins. Because a defect in DNA synthesis would be lethal, most of the replication mutants that have been studied are temperature-sensitive. Early replication mutants were isolated before the functions of the altered genes were known, and therefore were named dnaA, dnaB, and so forth. A major reason for the gaps in the alphabetical listing is that some genes were renamed when they were later shown to influence DNA synthesis indirectly rather than directly. For instance, the gene originally named dnaF was renamed nrdA when it was shown to be the structural gene for a subunit in ribonucleoside diphosphate reductase, the enzyme that converts ribonucleotides to deoxyribonucleotides.

    Important clues to replication gene function were obtained by determining the effects that temperature shifts have on DNA synthesis in conditional mutants. A mutant with a defect in an enzyme required for chain extension will stop DNA synthesis immediately after being switched from a permissive to a restrictive temperature. For this reason they are called quick-stop mutants. In contrast, a mutant with a defect in an enzyme required for the initiation of DNA replication will complete the ongoing round of DNA synthesis but will not initiate a new round. These mutants are called slow-stop mutants because they continue to synthesize DNA for some time after the temperature switch. As more was learned about the replication process and additional mutants were discovered investigators named the new genes according to their function. For instance, gyrA and gyrB, the structural genes for the two subunits in DNA gyrase, were named for their function. We will now turn our attention to the initiation stage of the replication process.