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G F Strniste

Publications and source records attributed to G F Strniste.

40 records · Page 3Linked to original sources

Development of bacteriophage alpha. II. Dependence on the host ribonucleic acid polymerase.

Measurements of ribonucleic acid (RNA) synthesis using (14)C-uracil uptake in rifampin-sensitive and rifampin-resistant strains of Bacillus megatherium were carried out after infection of the bacteria with bacteriophage alpha. Phage development was inhibited in the former but not the latter strain, showing that alpha phage development is dependent on the bacterial host RNA polymerase. This dependence exists at all times during eclipse. RNA polymerase extracts showed the same in vitro rifampin sensitivity as the corresponding bacterial strains.

Bacillus megaterium↗

Differential effects induced by N-hydroxy-2-acetylaminofluorene and N-hydroxy-2-aminofluorene in DNA excision-repair-deficient Chinese hamster cells.

The direct-acting cytotoxic properties of N-hydroxy-2-acetylaminofluorene (N-OH-AAF) and N-hydroxy-2-aminofluorene (N-OH-AF) have been determined in repair-proficient (AA8-4) and repair-deficient (UV-5) Chinese hamster ovary cells. Cytotoxicity comparisons indicate that UV-5 cells are considerably more sensitive to exposure to N-OH-AAF than is the parental AA8-4 cell line, i.e., concentrations needed to obtain a D37 for survival of AA8-4 is greater than 5-fold higher than for UV-5. Mutation analysis at the HGPRT locus also indicates the increased sensitivity of UV-5 cells to N-OH-AAF as witnessed by an enhanced induction of 6-thioguanine-resistant colonies at equitoxic doses. Conversely, N-OH-AAF, did not induce a 'UV-mimetic' response when comparing genotoxicity between these two cell lines. Our data coupled with previously published model-building and adduct removal studies (Broyde and Hingerty, 1983; Fuchs and Daune, 1974; Grunberger and Weinstein, 1976; Yamasaki et al., 1977) suggest that the minor DNA adduct species, N-(2'-deoxyguanosin-8-yl)-2-acetylaminofluorene, may be responsible for the hypermutagenicity witnessed in DNA excision-repair-deficient cells treated with N-OH-AAF.

2-Acetylaminofluorene↗