Elevated mutability of polA derivatives of Escherichia coli B/r at sublethal doses of ultraviolet light: evidence for an inducible error-prone repair system ("SOS repair") and its anomalous expression in these strains

Abstract

The SOS repair hypothesis proposes that UV-induced mutations in E. coli are caused by an inducible error-prone repair system (SOS repair) which is normally induced coordinately with such other recApluslexplus-dependent functions as filamentous growth, prophage induction and W-reactivation-2 in response to UV or other inhibitors of DNA synthesis. Since polA-l strains induce these functions at unusually low doses of UV, the SOS hypothesis predicts elevated UV mutability for such strains at these low doses (50 ergs per mm2 and below) Strain WP6, a polA-1 derivative of B/r, exhibits the predicted high UV mutability in this dose range, producing ten times as many Trp+ mutations as its polA+ counterpart, strain WP1, at a dose of 12.5 ergs per mm-2. The UV sensitivity of a lex polA double mutant, in which the lex and polA mutations fail to exert their individual effects on UV sensitivity additively, also confirms a prediction generated by the SOS hypothesis.--The uvrA polA-1 strain WP67 also shows elevated UV mutability at very low UV doses (5 ergs per mm-2 and below), producing about ten times as many Trp+ mutations at a dose of 0.6 ergs per mm-2 as its uvrA polA+ parent strain WP2s. It is proposed that the double mutant induces the SOS repair system (and probably other "reclex" inducible functions) at unusually low doses of UV as a consequence of its relatively inefficient repair of DNA damage when plated on broth-supplemented media.