Reference

Amplifications of phleomycin and bleomycin-induced antibiotic activity in Escherichia coli by aromatic cationic compounds

Amplifications of phleomycin and bleomycin-induced antibiotic activity in Escherichia coli by aromatic cationic compounds. Grigg, G. W.; Gero, Annette M.; Hughes, J. Margaret; Sasse, W. H. F.; Bliese, M.; Hart, N. K.; Johansen, O.; Kissane, P. (Mol. Cell. Biol. Unit., CSIRO, Epping, Australia). J. Antibiot., 30(10), 870-8 (English) 1977. CODEN: JANTAJ. ISSN: 0021-8820. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Interactions) A no. of arom. compds. enhanced the antibiotic activities of phleomycin [11006-33-0] and bleomycin [11056-06-7] on E.coli, including both DNA degrdn. and cell killing induced by the antibiotics. Detn. of the minimal structural requirements for potentiating activity indicated that all amplifiers contained 6-membered carbocyclic or heterocyclic arom. rings, were cationic or could acquire a pos. charge, and had areas exceeding those of simple monocyclic and bicyclic cations. Since the penetration and accumulation of many of these arom. compds. are specific for certain organisms or tissues, phleomycin-amplifier regimes may be selected in which the antibiotic effect is detd. by the properties of the particular amplifier involved.

Differential effects of UV protecting plasmid pKM101 and its derivative pGW16 on phleomycin sensitivity and mutagenesis in S

Differential effects of UV protecting plasmid pKM101 and its derivative pGW16 on phleomycin sensitivity and mutagenesis in S. typhimurium. Podger, Denis M.; Hall, Ruth M. (Div. Mol. Biol., CSIRO, North Ryde 2113, Australia). Mutat. Res., 140(2-3), 87-91 (English) 1984. CODEN: MUREAV. ISSN: 0027-5107. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Genetics) Section cross-reference(s): 4 The UV-protecting plasmid pKM101 and its mutant deriv. pGW16 were tested for their effects on phleomycin [11006-33-0] sensitivity and mutagenesis in S. typhimurium. Plasmid pGW16 retained the UV protection and some of the UV and Me methanesulfonate mutagenesis enhancement properties of pKM101 but lost the ability to enhance phleomycin, bleomycin, and g-radiation mutagenesis. Plasmid pGW16 also increased the sensitivity of the cells to the lethal effects of these treatments, in contrast to pKM101 whose presence conferred a slight resistance. The plasmid mucA and mucB genes required for phleomycin mutagenesis were shown in pGW16 to have lost some, but not all, of the muc functions. Apparently, in pGW16, the mutation may have affected mucA or mucB, leading to a loss of their protein products, or else another gene is defective in pGW16 that is required, in addn. to muc, for phleomycin- and g-radiation-induced mutagenesis.