Cornish K V, Pearlman R E
Mol Cell Biol. 1982 Aug;2(8):930-8. doi: 10.1128/mcb.2.8.930-938.1982.
Three mutant strains, one conditional, of Tetrahymena thermophila were defective in thymidine phosphorylating activity in vivo and in thymidine kinase activity in vitro. Nucleoside phosphotransferase activity in mutant cell extracts approached wild-type levels, suggesting that thymidine kinase is responsible for most, if not all, thymidine phosphorylation in vivo. Thymidine kinase activity in extracts of the conditional mutant strain was deficient when the cells were grown or assayed or both at the permissive temperature, implying a structural enzyme defect. Analysis of the reaction products from in vitro assays with partially purified enzymes showed that phosphorylation by thymidine kinase and nucleoside phosphotransferase occurred at the 5' position. Genetic analyses showed that the mutant phenotype was recessive and that mutations in each of the three mutant strains did not complement, suggesting allelism.
嗜热四膜虫的三个突变株（其中一个是条件突变株）在体内的胸苷磷酸化活性以及体外的胸苷激酶活性方面存在缺陷。突变细胞提取物中的核苷磷酸转移酶活性接近野生型水平，这表明胸苷激酶在体内负责大部分（如果不是全部）胸苷的磷酸化。当条件突变株的细胞在允许温度下生长、检测或两者同时进行时，其提取物中的胸苷激酶活性不足，这意味着存在结构酶缺陷。对部分纯化酶的体外检测反应产物的分析表明，胸苷激酶和核苷磷酸转移酶的磷酸化发生在5' 位。遗传分析表明，突变表型是隐性的，并且三个突变株中的每一个的突变都不能互补，这表明它们是等位基因。
