Ultraviolet Mutagenesis in Strains of E. coli deficient in DNA Polymerase

Abstract

CERTAIN mutations in Escherichia coli which cause increased sensitivity to ultraviolet light (UV) drastically change the UV mutability of the sensitive strain. Strains lacking the ability to excise pyrimidine dimers, for example, exhibit greatly increased UV mutability, producing induced mutations at doses of UV far smaller than those required to induce mutations in wild type strains^{1, 2}. Mutants owing their UV sensitivity to reduced ability to perform genetic recombination, on the other hand, show reduced mutability in response to UV compared with the wild type, and some (recA or exrA strains, for example) are stable to UV, producing no detectable induced mutations at any dose^3–5. Analysis of UV mutagenesis in such strains has led to the hypothesis that most UV-induced mutations in E. coli are errors in the recombinational repair of gaps in the daughter-strand which are located opposite unexcised pyrimidine dimers^{6, 7}.