Fisher C R, Malling H V, De Serres F J, Snyder S
Mutat Res. 1975 Dec;33(2-3):187-92. doi: 10.1016/0027-5107(75)90194-3.
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.
放线菌素D已知可与天然DNA结合，并且被广泛用作抗肿瘤剂以及DNA依赖性RNA和蛋白质合成的抑制剂。我们在此报告了放线菌素D在野生型粗糙脉孢菌中诱导产生需要紫色腺嘌呤的突变体（ad-3）。当该生物体在放线菌素D存在的情况下进行营养生长时，ad-3突变体的频率显著增加；突变频率至少为每106个存活个体中有3.6个。放线菌素D诱导的ad-3突变体中，29%为ad-3A，71%为ad-3B。ad-3B突变体根据互补模式分类为25%非极化互补；14%极化互补；以及61%非互补。放线菌素D诱导的突变体的互补类型谱与已知可诱导碱基对插入或缺失的ICR-170诱导的突变体、或X射线诱导的或自发突变体的互补类型谱最为相似。它与用亚硝酸或N-甲基-N'-硝基-N-亚硝基胍处理后观察到的谱显著不同，亚硝酸和N-甲基-N'-硝基-N-亚硝基胍是已知主要诱导碱基对替换的试剂。
