Mutagenicity of actinomycin D in Neurospora crassa.
Actinomycin D is known to bind to native DNA and is widely used as an antineoplastic agent and inhibitor of DNA-dependent RNA and protein synthesis. We report here the induction by actinomycin D of purple adenine-requiring mutants (ad-3) in wild-type Neurospora crassa. A significant increase in the frequency of ad-3 mutants was evident when the organism was grown vegetatively in the presence of actinomycin D; the mutation frequency was at least 3.6 per 106 survivors. The actinomycin D-induced ad-3 mutants were 29% ad-3A and 71% ad-3B. The ad-3B mutants were classed by complementation pattern as 25% nonpolarized complementing; 14% polarized complementing; and 61% noncomplementing. The spectrum of complementation types of the actinomycin D-induced mutants most closely parallels that of mutants induced by ICR-170, known to induce base-pair insertions or deletions, or that of X ray-induced or spontaneous mutants. It is significantly different from spectra seen following treatment with nitrous acid or N-methyl-N'-nitro-N-nitrosoguanidine, agents known to induce mainly base-pair substitutions.
D000225:Adenine / Q000378:metabolism; D003609:Dactinomycin / Q000633:toxicity*; D005796:Genes; D009153:Mutagens; D009154:Mutation; D009491:Neurospora / Q000187:drug effects*; D009492:Neurospora crassa / Q000187:drug effects* / Q000378:metabolism; D010858:Pigmentation
D009153:Mutagens; D003609:Dactinomycin; D000225:Adenine