Mutagens contribute to the human burden of heritable birth defects and cancer and probably to heart disease as well. Most mutagens in most organisms act by triggering a process called error-prone repair (EPR). Such mutagens' primary action is to damage DNA in ways that block the progress of the DNA replication complex. EPR then facilitates damage bypass in a poorly templated (and therefore mutagenic) manner. The bacteriophage T4 uvsX gene plays a central role in EPR and also in recombination. Its product is a recombinase, a protein that catalyzes homologous strand exchange between DNA molecules. The specific role of this protein in EPR remains mysterious. Although several severe mutations of uvsX are only semilethal, there are hints that an even more drastic disruption of uvsX might be fully lethal. Therefore, mutations were introduced into early parts of the gene and the resulting mutants were examined for phenotype, including viability. These mutants were not substantially different from the canonical uvsX mutant. This work is now in press and the project is completed.
