Yamaizumi M, Horwich A L, Ruddle F H
Mol Cell Biol. 1983 Apr;3(4):511-22. doi: 10.1128/mcb.3.4.511-522.1983.
To observe the effects of polyoma virus DNA on the expression of the herpes simplex virus (HSV) thymidine kinase (TK) gene early after transfer into TK-deficient mouse cells and the subsequent development of stable TK-positive transformants, we constructed a series of recombinant plasmids containing the herpes simplex virus TK gene joined with various segments of the polyoma virus genome and microinjected them into the nuclei or cytoplasm of LTK-A cells (TK(-), APRT(-)). The frequency of nucleus-injected cells expressing TK after 1 day, measured by autoradiography of cells incubated with [(3)H]thymidine, increased approximately 30-fold when the plasmids contained the polyoma virus origin of replication. The origin includes sequences with homology to the simian virus 40 origin of replication and adjoining sequences, including a recently defined transcription-enhancing sequence. After microinjection of a single origin-containing plasmid molecule per cell, TK expression was detected in approximately 50% of the injected cells. When a larger number of origin-containing plasmid molecules were injected per cell, all cells showed early TK activity. When the entire polyoma virus early region was present, neighboring uninjected cells became TK positive. When plasmids were injected into the cell cytoplasm, approximately 400 times as many molecules per cell were needed to cause early TK activity. The frequency of stable transformation observed 2 weeks after nuclear injection of 10 to 20 polyoma virus origin-containing plasmid molecules per cell was at least 2 orders of magnitude greater than with plasmids containing the TK gene alone. The greatest enhancement of stable TK transformation was obtained with plasmids containing the origin alone, when the maximum frequency of stable transformation was 5%. The addition of the coding regions for the small and medium T antigens or the entire early region significantly decreased TK transformation frequency in a copy-dependent fashion. The timing of stabilization of TK-positive transformation was analyzed by releasing hypoxanthine-aminopterin-thymidine selection pressure at various times after microinjection, culturing the cells in nonselective medium, and assaying for TK activity. Stabilization was found to occur between 3 and 6 days after nuclear injection. Cells injected with a plasmid containing the origin and the early region were examined for expression of the large T antigen with polyoma virus antitumor serum and immunofluorescent staining. The expression of the large T antigen was clearly associated with a cytopathic effect. TK-positive clones observed 2 weeks after injection of the plasmid were uniformly T antigen negative. Cytotoxicity may be the result of plasmid replication and toxic levels of T antigen or TK. In addition, expression of the large T antigen may block stabilization by preventing the integration of origin-containing plasmid molecules.
为了观察多瘤病毒DNA在转入TK缺陷型小鼠细胞后早期对单纯疱疹病毒(HSV)胸苷激酶(TK)基因表达的影响以及随后稳定的TK阳性转化体的形成,我们构建了一系列重组质粒,这些质粒含有与多瘤病毒基因组不同片段相连的单纯疱疹病毒TK基因,并将它们显微注射到LTK - A细胞(TK(-),APRT(-))的细胞核或细胞质中。通过用[³H]胸苷孵育细胞的放射自显影法测量,在注射后1天表达TK的细胞核注射细胞的频率,当质粒含有多瘤病毒复制起点时增加了约30倍。该起点包括与猿猴病毒40复制起点具有同源性的序列以及相邻序列,包括最近定义的转录增强序列。在每个细胞显微注射单个含起点的质粒分子后,在约50%的注射细胞中检测到TK表达。当每个细胞注射大量含起点的质粒分子时,所有细胞都显示出早期TK活性。当存在整个多瘤病毒早期区域时,相邻的未注射细胞变为TK阳性。当质粒注射到细胞质中时,每个细胞需要大约400倍数量的分子才能引起早期TK活性。在每个细胞核注射10至20个含多瘤病毒起点的质粒分子2周后观察到的稳定转化频率比单独含有TK基因的质粒至少高2个数量级。单独含有起点的质粒获得了最大程度的稳定TK转化增强,此时稳定转化的最大频率为5%。添加中小T抗原的编码区或整个早期区域以拷贝依赖的方式显著降低了TK转化频率。通过在显微注射后的不同时间释放次黄嘌呤 - 氨基蝶呤 - 胸腺嘧啶选择压力、在非选择培养基中培养细胞并检测TK活性,分析了TK阳性转化体稳定化的时间。发现稳定化发生在核注射后3至6天之间。用多瘤病毒抗肿瘤血清和免疫荧光染色检查注射了含起点和早期区域质粒的细胞中大T抗原的表达。大T抗原的表达明显与细胞病变效应相关。注射质粒2周后观察到的TK阳性克隆均为T抗原阴性。细胞毒性可能是质粒复制以及T抗原或TK的毒性水平的结果。此外,大T抗原的表达可能通过阻止含起点的质粒分子整合来阻断稳定化。