Wachter M, Riedle G, Henning R
J Virol. 1985 Nov;56(2):520-6. doi: 10.1128/JVI.56.2.520-526.1985.
The formation of oligomers of simian virus 40 (SV40) large T antigen in SV40-infected and -transformed monkey cells was analyzed by sucrose density gradient centrifugation. The overall distribution of total T antigen during lytic infection showed mainly low-molecular-weight forms (monomers and dimers) in the early phase (10 h postinfection) and an increase in the number of oligomers in the late phase of the lytic cycle (36 h postinfection), indicating an accumulation of these final products. In contrast, studying the conversion of newly synthesized T antigen into oligomers by appropriate pulse-chase radiolabeling of infected cells revealed that this processing decelerates considerably during the late phase of infection. This mechanism can be reaccelerated by blocking DNA replication with aphidicolin. Since none of these results could be obtained by using synchronized SV40-transformed monkey cells (COS-1), these observations are compatible with the idea that the process of T antigen oligomerization may be involved in viral, but not in cellular, DNA synthesis.
通过蔗糖密度梯度离心法分析了猴空泡病毒40(SV40)感染和转化的猴细胞中SV40大T抗原寡聚体的形成情况。在裂解感染期间,总T抗原的总体分布显示,在早期阶段(感染后10小时)主要是低分子量形式(单体和二聚体),而在裂解周期后期(感染后36小时)寡聚体数量增加,表明这些终产物在积累。相比之下,通过对感染细胞进行适当的脉冲追踪放射性标记来研究新合成的T抗原向寡聚体的转化,结果显示在感染后期这种加工过程显著减慢。用阿非科林阻断DNA复制可使这一机制重新加速。由于使用同步化的SV40转化猴细胞(COS-1)无法得到这些结果,因此这些观察结果与T抗原寡聚化过程可能参与病毒而非细胞DNA合成的观点相符。