Affiliation:
1. Genetic Toxicity Branch, Division of Toxicology, Food and Drug Administration, Department of Health, Education, and Welfare, Washington, D.C. 20204
Abstract
N
-Methyl-
N
′-nitro-
N
-nitrosoguanidine (MNNG) induces cycloheximide-resistant mutations in
Saccharomyces cerevisiae
, but few, if any, resistant mutants are induced by the acridine mustard ICR-170. Cycloheximide sensitivity in yeast is associated with the ribosome, and treatment with the antibiotic at concentrations of 2 μg/ml results in complete inhibition of protein synthesis. Missense mutations induced by MNNG probably lead to the loss of cycloheximide binding sites on the ribosome, resulting in resistance to the antibiotic without altering the activity of the organelle in protein synthesis. ICR-170, however, induced primarily frameshift mutations that would alter ribosome structural integrity, resulting in cell death rather than resistance. ICR-170 and MNNG are both mutagenic in a system in which base-pair substitution and frameshift mutations can be detected. These results indicate that cycloheximide resistance in
S. cerevisiae
, like streptomycin and spectinomycin resistance in
Escherichia coli
, can be induced by base-pair substitution mutagens but not by frameshift mutagens such as ICR-170.
Publisher
American Society for Microbiology
Subject
Molecular Biology,Microbiology
Reference3 articles.
1. Frameshift mutagenesis in Salmonella;Ames B. N.;Cold Spring Harbor Symp. Quant. Biol.,1966
2. Berger H. W. Brammar and C. Yanofsky. 1968. Spontaneous and ICR-191-A-induced frameshift mutations in the A gene of Escherichia coli tryptophan synthe
3. TABLE 4. Induction of canR mutants in log- and stationary-phase starved cells of S. cerevisiae by ICR-170.Ea
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