ArticleIida K, Koike M.
Microbiol Immunol. 1977;21(9):481-94.
Antibacterial activities of 3-di(hydroxymethyl) amino-6[2-(5-nitro-2-furyl)vinyl]-1,2,4-triazine, (dihydroxymethyl furatrizine) were investigated using mutant strains of Escherichia coli lacking repair systems for DNA damage, i.e. polA, uvrA, uvrA, uvrC, recA, recB, recC and uvrArecA. All of the mutant strains were more sensitive to the drug than the parent sgrains, as was the case with the sensitivity to UV-irradiation. These results indicate that the drug acts lethally on sensitive bacteria by damaging their DNA, and parts of the damaged DNA are repaired by excision and recombinational repair systems. Filamentous cell formation was induced in all strains except the uvrArecA strain by sublethal concentration of the drug, as well as by UV-irradiation. It is possible that the occurrence of the short period of "unbalanced growth" induced by such DNA damaging agents leads to filament formation. In the cells of the double mutant, filament formation was induced by the drug but not by UV-irradiation, and the majority of the filamentous cells formed were multinucleated. This suggests that, in this double mutant, the drug directly reacts with the septation mechinery of the cell envelope, resulting in filament formation. This hypothesis is supported by the electron microscopic observations that septation is interrupted in the filamentous cells induced by the drug.