通过抑制性tRNA基因对单纯疱疹病毒胸苷激酶基因无义突变在哺乳动物细胞中的功能抑制
Functional suppression in mammalian cells of nonsense mutations in the herpes simplex virus thymidine kinase gene by suppressor tRNA genes.
作者信息
Summers W P, Summers W C, Laski F A, RajBhandary U L, Sharp P A
出版信息
J Virol. 1983 Aug;47(2):376-9. doi: 10.1128/JVI.47.2.376-379.1983.
Abstract
A nonsense mutation (UAG) in the thymidine kinase gene of herpes simplex virus type 1 can be suppressed in vivo to produce active thymidine kinase by prior infection with a defective simian virus 40 stock which acts as a vector to introduce a functional suppressor tRNA gene into mammalian cells in culture. The suppression is specific for UAG, but not UGA or missense, mutants and restores thymidine kinase activity to 20 to 40% of the wild-type level. These results suggest that many cell lines susceptible to simian virus 40 infection may be transiently converted to a suppressor-positive phenotype for use in the genetic study of mammalian viruses.
摘要
单纯疱疹病毒1型胸苷激酶基因中的无义突变（UAG），可通过事先用缺陷型猿猴病毒40毒株感染在体内被抑制，从而产生活性胸苷激酶。该毒株作为载体，将功能性抑制性tRNA基因导入培养的哺乳动物细胞中。这种抑制作用对UAG突变体具有特异性，对UGA或错义突变体则无作用，可将胸苷激酶活性恢复至野生型水平的20%至40%。这些结果表明，许多易受猿猴病毒40感染的细胞系可能会暂时转变为抑制阳性表型，用于哺乳动物病毒的遗传学研究。
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