Slow excision repair in an mfd mutant of Escherichia coli B/r.

Abstract

A mutant of Escherichia coli B/r designated mfd is very deficient in the ability to exhibit “mutation frequency decline”, the characteristic loss of potential suppressor mutations which occurs when protein synthesis is briefly inhibited after irradiation with ultraviolet light (UV). This mutant is known to excise pyrimidine dimers at an abnormally slow rate, although it is as UV-resistant as its mfd+ B/r parent strain. We have found that the mfd mutant performs the initial incision step of excision repair normally, but repairs the resulting single-strand breaks much more slowly than the mfd+ strain. We conclude that the mfd mutant performs the excision step of pyrimidine dimer excision inefficiently, but our data do not rule out the possibility that one or more subsequent steps of repair may also be slow. In spite of the slow dimer excision in the mfd mutant, single-strand DNA breaks do not accumulate during post-irradiation incubation, implying that incision and excision are well coordinated. The prolonged post-irradiation lag in cell division and DNA synthesis which accompany slow excision in the mfd strain indicates that resumption of these processes at optimal rates is linked to the timing of excision repair. The normal UV-resistance of the mfd mutant also suggests such coordination and shows that the rate of excision repair is independent of its ultimate efficiency.