Rosenthal L J, Brown M
Nucleic Acids Res. 1977 Mar;4(3):551-65. doi: 10.1093/nar/4.3.551.
The transition from early to late transcription of SV40 DNA in productively infected BSC-1 cells was analyzed using both inhibitors of DNA replication, and early (Group A) temperature sensitive (ts) mutants of SV40. Late virus specific cytoplasmic RNA sedimenting at 16S in neutral sucrose gradients and complementary to the plus (L) DNA strand of SV40 was detected in cultures infected in the presence of three inhibitors of DNA replication (Ara-C, FdU, and chloroquine), even though the inhibition of viral DNA replication appeared to be essentially complete. After infection with the early SV40 mutant tsA58, no DNA replication was detected at the restrictive temperature (41 degrees C) and no significant late RNA complementary to the plus (L) strand was found, in either the cytoplasm or nuclei of infected cells. These data support the concept that expression of late viral functions requires the initiation of viral DNA synthesis or a functional gene A protein, or both.
利用DNA复制抑制剂以及SV40早期（A组）温度敏感（ts）突变体，分析了在被有效感染的BSC-1细胞中SV40 DNA从早期转录向晚期转录的转变。在存在三种DNA复制抑制剂（阿糖胞苷、氟脱氧尿苷和氯喹）的情况下感染的培养物中，检测到晚期病毒特异性细胞质RNA，其在中性蔗糖梯度中沉降系数为16S，并且与SV40的正（L）DNA链互补，尽管病毒DNA复制的抑制似乎基本完全。用早期SV40突变体tsA58感染后，在限制温度（41℃）下未检测到DNA复制，并且在感染细胞的细胞质或细胞核中均未发现与正（L）链互补的大量晚期RNA。这些数据支持这样的概念，即晚期病毒功能的表达需要病毒DNA合成的起始或功能性A基因蛋白，或两者都需要。
