Hartzell S W, Yamaguchi J, Subramanian K N
Nucleic Acids Res. 1983 Mar 11;11(5):1601-16. doi: 10.1093/nar/11.5.1601.
We have constructed deletion mutants of simian virus 40 (SV40) lacking the two tandemly repeated copies or all three copies of the 21-bp repeated sequence located in the origin region. The mutants were viable, but had lower infectivities compared to the wild type. The mutant lacking two copies of the 21-bp repeat grew fairly well indicating that the one copy of the 21-bp repeat it contains is adequate. The other mutant lacking all the three copies of the 21-bp repeat was also viable but grew poorly. The viability of this mutant suggests that the upstream 72-bp repeated sequence compensates, though only partially, for the absence of the 21-bp repeat. The growth deficiencies of the deletion mutants could not be overcome by complementation with temperature-sensitive helper mutants providing either the early or the late functions of the virus, suggesting that the deficiencies lie in both early and late gene expression and/or in replication.
我们构建了猿猴病毒40（SV40）的缺失突变体，这些突变体缺失了位于起始区域的21碱基对重复序列的两个串联重复拷贝或所有三个拷贝。这些突变体是有活力的，但与野生型相比感染力较低。缺失两个21碱基对重复拷贝的突变体生长得相当好，这表明它所含的一个21碱基对重复拷贝就足够了。另一个缺失所有三个21碱基对重复拷贝的突变体也是有活力的，但生长不良。这个突变体的活力表明上游72碱基对重复序列虽然只是部分地补偿了21碱基对重复序列的缺失。缺失突变体的生长缺陷不能通过与提供病毒早期或晚期功能的温度敏感辅助突变体互补来克服，这表明缺陷存在于早期和晚期基因表达和/或复制中。
