Theile M, Scherneck S, Geissler E
Mutat Res. 1976 Oct;37(1):111-23. doi: 10.1016/0027-5107(76)90059-2.
The mutagenic action of SV40 in permanent lines of Chinese hamster cells (CHO-K1 and V79) was investigated with the aid of different resistance markers. The markers studied had resistance to 8-azaguanine (25 and 30 mug/ml), aminopterin (3.3--5.5X10(-3) mug/ml), colchicine (6.5 and 7.0X10(-2) mug/ml) and 5-bromodeoxyuridine (50--120 mug/ml), respectively. After virus infection the mutation frequencies were increased by one (azaguanine, aminopterin) and two (colchicine) orders of magnitude as compared with spontaneous mutation frequencies. In contrast, it was not possible to enhance the frequency of mutation to BUdR resistance. On the other hand, the ability to proliferate in HAT medium was induced in three of five BUdR-resistant cell clones by infection with SV40. The resistance induced by SV40 was stable when isolated clones were cultured under non-selective conditions. Mechanisms are proposed that may be responsible for the mutagenic action of SV40.
借助不同的抗性标记，研究了猴空泡病毒40（SV40）对中国仓鼠细胞永久系（CHO - K1和V79）的诱变作用。所研究的标记分别对8 - 氮杂鸟嘌呤（25和30微克/毫升）、氨基蝶呤（3.3 - 5.5×10⁻³微克/毫升）、秋水仙碱（6.5和7.0×10⁻²微克/毫升）和5 - 溴脱氧尿苷（50 - 120微克/毫升）具有抗性。病毒感染后，与自发突变频率相比，突变频率增加了一个数量级（氮杂鸟嘌呤、氨基蝶呤）和两个数量级（秋水仙碱）。相比之下，无法提高对5 - 溴脱氧尿苷抗性的突变频率。另一方面，通过SV40感染，在五个抗5 - 溴脱氧尿苷细胞克隆中的三个中诱导出了在次黄嘌呤 - 氨基蝶呤 - 胸腺嘧啶核苷（HAT）培养基中增殖的能力。当分离的克隆在非选择性条件下培养时，SV40诱导的抗性是稳定的。提出了可能与SV40诱变作用有关的机制。
