Filament Formation in Ultraviolet-Resistant Mutants of Escherichia coli Strain B 3

Abstract

At low doses, ultraviolet light (UV) inhibits cell division and induces filament formation during postirradiation growth in Escherichia coli strain B (1, 2). This strain is considered to have an enzyme for the repair of UV-induced damage to DNA but not cell division (2-5). Mutants selected for resistance, on the other hand, are presumed to have mechanisms for the repair of injury to cell division, since they do not form filaments on irradiation (1, 6-8). Correlation between this property and UV sensitivity has been established in a number of genetic studies. Present evidence indicates that there are two genetic loci, fil and lon, which control filament formation in E. coli and that mutation at any one of these sites affects radiation sensitivity of the organism (9-12). In addition to the properties described above, several phenotypic differences have been found among the radiation-resistant mutants on the basis of crossresistance to radiomimetic compounds, metabolic inhibitors, mutagens, and Xrays (13-20). Perhaps the best evidence is provided by the studies of Curryl and Greenberg (21), who showed that the UV resistance was not always associated with the resistance to filament formation. They observed that, in E. coli strain S, the mutants selected for resistance to l-chloropropyl-3-nitro-l-nitrosoguanidine and nitromin showed cross-resistance to UV, but retained their ability to form filaments on irradiation.