Glebov O K, Abramian D S, Tomilin N V
Tsitologiia. 1985 May;27(5):572-81.
Analysis was made of the phenotype stability of some clones of thymidine kinase deficient (TK-) Chinese hamster cells transformed by thymidine kinase gene (TK-gene) of Herpes simplex virus type (HSV 1). The presence of a fragment of human satellite DNA III in the plasmid DNA carrying the TK-gene of HSV 1 reduced notably the rate of the loss of TK+-phenotype, and the treatment of the cells with a tumour promoter--12-o-tetradecanoyl-phorbol-13-acetate--immediately after transformation destabilizes TK+-phenotype of transformant clones. Removal of the eukaryotic carrier DNA for the plasmid DNA without the TK-gene of HSV 1 destabilizes the clone transformant phenotype. Changes in the structure of the plasmid DNA containing no TK-gene of HSV 1 and introduced into cells simultaneously with TK-gene containing plasmids affects the rate of the loss of TK+-phenotype transformed cells.
对一些由单纯疱疹病毒1型(HSV 1)的胸苷激酶基因(TK基因)转化的胸苷激酶缺陷(TK-)中国仓鼠细胞克隆的表型稳定性进行了分析。携带HSV 1的TK基因的质粒DNA中存在人卫星DNA III片段,显著降低了TK+表型丧失的速率,并且在转化后立即用肿瘤促进剂——12-o-十四烷酰佛波醇-13-乙酸酯——处理细胞会使转化克隆的TK+表型不稳定。去除不含HSV 1的TK基因的质粒DNA的真核载体DNA会使克隆转化体表型不稳定。不含HSV 1的TK基因且与含TK基因的质粒同时导入细胞的质粒DNA结构变化会影响转化细胞TK+表型丧失的速率。