Cornelis J J, Lupker J H, Klein B, van der Eb A J
Mutat Res. 1981 Jun;82(1):1-10. doi: 10.1016/0027-5107(81)90132-9.
The induction of phenotypic wild-type revertants in the progeny of an unirradiated or UV-irradiated temperature-sensitive late mutant of simian virus 40 was studied after low multiplicity passages in normal or UV-irradiated confluent monkey kidney cells. The production of wild-type revertants in the progeny of undamaged tsBC245 was followed by infecting the cells at distinct times after irradiation of the cells. Mutation frequencies reached a maximum when infection was delayed for 3--4 days after irradiation of the host cells, and declined gradually thereafter. Virus grown in unirradiated cells did not show such an alteration in mutation frequency. The temporarily higher mutation frequency of virus in UV-pretreated cells is due to a transient mutator activity operating in these cells rather than to an increased number of replications performed in UV-irradiated cells. A similar time course was found for the reactivation of UV-damaged SV40. This might suggest that reactivation and mutagenesis are manifestations of the same process. The yield of mutants due to irradiation of the virus alone was enhanced when infection was delayed for some days after the cells reached confluency; UV pretreatment of the host cells did not enhance the level of mutation obtained by UV irradiation of the virus.
在正常或紫外线照射的汇合猴肾细胞中进行低倍传代后,研究了未照射或紫外线照射的猿猴病毒40温度敏感晚期突变体子代中表型野生型回复体的诱导情况。在细胞照射后不同时间感染细胞,追踪未受损的tsBC245子代中野生型回复体的产生。当宿主细胞照射后感染延迟3 - 4天时,突变频率达到最大值,此后逐渐下降。在未照射细胞中生长的病毒未显示出这种突变频率的变化。紫外线预处理细胞中病毒的突变频率暂时升高是由于这些细胞中存在短暂的诱变活性,而不是由于在紫外线照射细胞中进行的复制次数增加。对于紫外线损伤的SV40的复活,也发现了类似的时间进程。这可能表明复活和诱变是同一过程的表现。当细胞达到汇合后感染延迟数天时,仅病毒照射产生的突变体产量会增加;宿主细胞的紫外线预处理并未提高病毒紫外线照射获得的突变水平。