Summers W C, Sarkar S N, Glazer P M
Radiobiology Laboratories, Yale University, New Haven, Connecticut 06510.
Cancer Surv. 1985;4(3):517-28.
The understanding of mutagenic mechanisms in mammalian cells is based on extrapolations of results obtained in prokaryotes and simple eukaryotes. The use of animal viruses as targets for mutagenesis suggests that these extrapolations may be valid: recent data indicate that mutagenesis of ultraviolet-damaged templates in mammalian cells seems to occur at similar sites to that observed in prokaryotes; furthermore, nuclear replicating animal viruses are subject to the phenomenon of ultraviolet-enhanced reactivation, called SOS reactivation in bacteria. In experiments analogous to Weigle mutagenesis of phage, several groups have shown that animal cells appear to respond to DNA damage by induction of mutagenic pathways which can act upon infecting viral genomes. Recent experiments with shuttle vectors that can replicate both in animal cells and in bacteria have confirmed these conclusions. These vectors now make possible the rapid recovery of mutant genes for direct sequence analysis.
对哺乳动物细胞致突变机制的理解是基于对原核生物和简单真核生物中所获结果的推断。将动物病毒用作诱变靶点表明这些推断可能是有效的：最近的数据表明，哺乳动物细胞中紫外线损伤模板的诱变似乎发生在与原核生物中观察到的类似位点；此外，核复制动物病毒会受到紫外线增强再活化现象的影响，这种现象在细菌中称为SOS再活化。在类似于噬菌体韦格勒诱变的实验中，几个研究小组表明，动物细胞似乎通过诱导可作用于感染病毒基因组的诱变途径来响应DNA损伤。最近使用可在动物细胞和细菌中都能复制的穿梭载体进行的实验证实了这些结论。这些载体现在使得能够快速回收突变基因以进行直接序列分析。
