Halpern M E, Smiley J R
J Virol. 1984 Jun;50(3):733-8. doi: 10.1128/JVI.50.3.733-738.1984.
We have transferred two deletions affecting the 5' end of the herpes simplex virus thymidine kinase (TK) gene into the intact viral genome. One, extending from -12 to +189, had no effect on TK mRNA synthesis and only a small effect on TK activity, although the first 27 codons of the TK polypeptide were deleted. The other, extending from -85 to +85, severely impaired TK mRNA synthesis. We conclude that the amino terminus of the TK polypeptide is dispensable for catalytic activity, and that expression of TK in viral infections requires some of the same promoter elements used in uninfected cells.
我们已将两个影响单纯疱疹病毒胸苷激酶(TK)基因5'端的缺失片段导入完整的病毒基因组。其中一个缺失片段从-12延伸至+189,对TK mRNA的合成没有影响,对TK活性仅有轻微影响,尽管TK多肽的前27个密码子被删除。另一个缺失片段从-85延伸至+85,严重损害了TK mRNA的合成。我们得出结论,TK多肽的氨基末端对于催化活性是可有可无的,并且在病毒感染中TK的表达需要一些未感染细胞中使用的相同启动子元件。