Davidson R L, Adelstein S J, Oxman M N
Proc Natl Acad Sci U S A. 1973 Jul;70(7):1912-6. doi: 10.1073/pnas.70.7.1912.
Thymidine kinase (EC 2.7.1.21)-deficient mouse cells were infected with inactivated herpes simplex virus, after which "transformed" cells that produce viral thymidine kinase were isolated. Shortly after transformation, the expression of the viral enzyme could be suppressed and reactivated with high efficiency. On continued multiplication in nonselective medium, the proportion of cells producing the viral enzyme decayed exponentially. This decay seemed to represent a change in the expression of the viral gene for thymidine kinase rather than the loss of the gene from the cells, since the viral enzyme could be apparently reactivated in every cell, albeit at a very low frequency.
用灭活的单纯疱疹病毒感染胸苷激酶（EC 2.7.1.21）缺陷的小鼠细胞，之后分离出产生病毒胸苷激酶的“转化”细胞。转化后不久，病毒酶的表达能够被高效抑制并重新激活。在非选择性培养基中持续增殖时，产生病毒酶的细胞比例呈指数衰减。这种衰减似乎代表胸苷激酶病毒基因表达的变化，而非该基因从细胞中丢失，因为病毒酶显然能在每个细胞中重新激活，尽管频率很低。
