Complementation studies with the repair-deficient uvrD3, uvrE156, and recL152 mutations in Escherichia coli.

Previous work showed that the mutations uvrD3, uvrE156, and recL152 were closely linked and increased UV-sensitivity. They were phenotypically distinguishable in that only the uvrD3 mutation significantly decreases host cell reactivation of UV-irradiated phage (Hcr-) and repair of methylmethane sulfonate (MMS)-induced damage, and only the uvrE156 mutation increased mutation rates (Mut-). MMS-resistant revertants of a uvrD3 mutant were still UV-sensitive and fell into two phenotypic classes. Hcr- Mut+ (non-mutator) and Hcr+ Mut-. In this work complementation tests were done by examining UV- and MMS-sensitivity and host cell reactivation in heterogenotes containing combinations of uvrD3, uvrE156, recL152, and the MMS-resistant mutations derived from uvrD3. The mutations could not complement each other in the repair of UV-damage, the one trait all had in common, indicating that they were in one gene. For the most part, the different mutations were able to complement each other in respect to traits in which one was deficient and the other had wild type activity.