René B, Auclair C, Paoletti C
Biochem Biophys Res Commun. 1986 Jul 31;138(2):505-11. doi: 10.1016/s0006-291x(86)80525-3.
The simple reversible intercalating agents isopropyl-oxazolopyridocarbazole and 9-aminoacridine have been found to induce frameshift -1 mutations at a much lower level in Salmonella typhimurium delta uvrB TA 1537 than in the uvr+ wild type TA 1977 strain. This phenomenon can neither be explained by differential cytotoxicity of the drug nor by selective permeation and accessibility to intercalating sites to bacterial DNA. These finding indicate that the lower mutagenicity of intercalating agents in the delta uvrB strains does not result from nonspecific phenotypic modifications of parameters which control the mutagenesis. That leads to the hypothesis that in agreement with the Streisinger's model, the excision repair system could be directly involved in the appearance of frameshift mutations.
已发现简单的可逆嵌入剂异丙基 - 恶唑并吡啶咔唑和9 - 氨基吖啶在鼠伤寒沙门氏菌ΔuvrB TA 1537中诱导移码 -1突变的水平比uvr +野生型TA 1977菌株低得多。这种现象既不能用药物的差异细胞毒性来解释，也不能用对细菌DNA嵌入位点的选择性渗透和可及性来解释。这些发现表明，嵌入剂在ΔuvrB菌株中较低的诱变性并非源于控制诱变的参数的非特异性表型修饰。这导致了一个假设，即与施特赖辛格模型一致，切除修复系统可能直接参与移码突变的出现。
