Sarasin A, Benoit A
Mutat Res. 1980 Mar;70(1):71-81. doi: 10.1016/0027-5107(80)90059-7.
The survival of UV-irradiated simian virus 40 (SV40) on UV-irradiated monkey kidney CV-1P cells at 33 degrees was increased over survival on unirradiated cells. During this process - called induced-virus reactivation - the progeny virus yielded by UV-irradiated cells had a much higher mutation frequency than did the progeny from unirradiated cells. Mutation rates were quantified by using phenotypic reversion towards wild-type growth of an early (tsA 58) or a late (tsB 201) temperature-sensitive SV40 mutant. Analysis of SV40 revertant genomes indicated that no detectable deletions of additions were responsible for the reversion process. These results suggest that enzymes from UV-irradiated cells are able to replicate UV-irradiated DNA by an error-prone mode of DNA repair. Induced virus reactivation and error-prone replication are probably one of the expressions of SOS functions in mammalian cells.
紫外线照射的猴空泡病毒40(SV40)在33摄氏度下于紫外线照射的猴肾CV-1P细胞上的存活率高于在未照射细胞上的存活率。在这个被称为诱导病毒复活的过程中,紫外线照射细胞产生的子代病毒的突变频率比未照射细胞产生的子代病毒高得多。通过使用早期(tsA 58)或晚期(tsB 201)温度敏感型SV40突变体向野生型生长的表型回复来量化突变率。对SV40回复基因组的分析表明,回复过程中没有可检测到的缺失或插入。这些结果表明,紫外线照射细胞中的酶能够通过易错的DNA修复模式复制紫外线照射的DNA。诱导病毒复活和易错复制可能是哺乳动物细胞中SOS功能的表达之一。