Ohta T, Nakamura N, Moriya M, Shirasu Y, Kada T
Mutat Res. 1984 Mar-Apr;131(3-4):101-9. doi: 10.1016/0167-8817(84)90048-8.
The SOS-function-inducing activities of 42 chemical mutagens were investigated in Escherichia coli K12. The induction of the SOS function was assayed by monitoring the beta-galactosidase activity in the sulA::lacZ fusion strain PQ37 . To correct for the inhibitory effects of test chemicals on mRNA or protein synthesis, the level of the constitutive alkaline phosphatase was assayed in parallel. Most of the mutagens reported to be mutagenic to the Ames' Salmonella tester strains showed the SOS-function-inducing activity. The inducible SOS repair may be responsible for not only base-change mutations but also frameshift mutations. However, 9-aminoacridine, ethidium bromide and 4-nitro-o-phenylenediamine did not induce the SOS function, suggesting that the mutagenesis induced by these mutagens may occur independently of SOS repair. Present results support the SOS mutagenesis model that error-prone SOS repair plays an important role in mutagenesis induced by most chemical mutagens.
在大肠杆菌K12中研究了42种化学诱变剂的SOS功能诱导活性。通过监测sulA::lacZ融合菌株PQ37中的β-半乳糖苷酶活性来检测SOS功能的诱导情况。为校正测试化学品对mRNA或蛋白质合成的抑制作用，同时检测组成型碱性磷酸酶的水平。大多数据报道对艾姆斯沙门氏菌测试菌株具有诱变性的诱变剂都表现出SOS功能诱导活性。诱导性SOS修复可能不仅与碱基变化突变有关，还与移码突变有关。然而，9-氨基吖啶、溴化乙锭和4-硝基邻苯二胺未诱导SOS功能，这表明这些诱变剂诱导的诱变可能独立于SOS修复发生。目前的结果支持SOS诱变模型，即易错SOS修复在大多数化学诱变剂诱导的诱变中起重要作用。
