Three loci in Escherichia coli K-12 that control the excision of pyrimidine dimers and certain other mutagen products from DNA.

LTRAVIOLET irradiation produces dimers of thymine, thymine-cytosine and cytosine in deoxyribonucleic acid (DNA) (BEUKERS, IJLSTRA and BERENDS 1960; WACKER, DELLWEG and WEINBLUM 1960; SETLOW, CARRIER and BOLLUM 1965). UV light inactivates transforming DNA and induces thymine dimers in a parallel manner, as if the dimers block transforming activity (SETLOW and SETLOW 1962). Thymine dimers and thymine-cytosine dimers are removed and probably monomerized by photoreactivation enzyme ( WULF and RUPERT 1962; SETLOW, CARRIER and BOLLUM 1965). They are excised from DNA during incubation in the dark in wild-type strains of E. coli. However, this excision does not occur in the radiosensitive mutants Bs.l and K-12 uvrA (SETLOW and CARRIER 1964; BOYCE and HOWARD-FLANDERS 1964a). T1 or A bacteriophage irradiated with ultraviolet light (UV) form more plaques when plated on wild-type cells than when plated on these radiosensitive mutants (ELLISON. FEINER and HILL 1960; HOWARD-FLANDERS, BOYCE, SIMSON and THERIOT 1962; RORSCH, EDELMAN and COHEN 1963; HARM 1963). These results may be explained if the irradiated phage DNA is reactivated (host cell reactivation) in wild-type hosts, but not in these UV-sensitive mutants. The reactivation of UV-irradiated T1 bacteriophage is controlled by three genetic loci, designated uLv-A, uvrB and uurC. the approximate map positions of which have been reported (HOWARD-FLANDERS 1964; VAN DE PUTTE, VAN SLUIS, VAN DILLEWIJN and RORSCH 1965). In the present paper, we report the genetic analysis of 23 such mutants, more accurate mapping by cotransduction of the uurA, uurB and the uurC loci with other markers, some properties of the double mutants that carry two uur mutations, and evidence that all three loci control the excision from DNA of UV-induced thymine dimers and thymine-cytosine dimers.