Summers W P, Wagner M, Summers W C
Proc Natl Acad Sci U S A. 1975 Oct;72(10):4081-4. doi: 10.1073/pnas.72.10.4081.
Mutations in the viral gene coding for the thymidine kinase (ATP:thymidine 5'-phosphotransferase, EC 2.7.1.75) induced by herpes simplex virus have been obtained by selection of virus resistant to bromodeoxyuridine when grown in thymidine-kinase-deficient LMTK- mouse cells. Proteins labeled after infection of Vero (monkey) cells with herpes simplex virus were analyzed by gel electrophoresis and one protein of about 40,000 daltons was consistently altered in a number of thymidine-kinase-deficient mutants. Many viral mutants lacked this peptide and one class of these mutants induced the synthesis of new shorter peptides. Revertant virus could be selected which simultaneously regained the ability to induce thymidine kinase activity, regained the intact thymidine kinase peptide, and lost the ability to synthesize the shorter peptide fragment. These mutants comprise a class of animal virus mutants which have the properties expected of peptide chain termination mutants.
通过在胸苷激酶缺陷的LMTK-小鼠细胞中培养时选择对溴脱氧尿苷耐药的病毒，已获得单纯疱疹病毒诱导的胸苷激酶（ATP：胸苷5'-磷酸转移酶，EC 2.7.1.75）编码病毒基因的突变体。用单纯疱疹病毒感染Vero（猴）细胞后标记的蛋白质通过凝胶电泳进行分析，在许多胸苷激酶缺陷突变体中，一种约40,000道尔顿的蛋白质持续发生改变。许多病毒突变体缺乏这种肽，其中一类突变体诱导合成新的较短肽。可以选择回复病毒，其同时恢复诱导胸苷激酶活性的能力，重新获得完整的胸苷激酶肽，并丧失合成较短肽片段的能力。这些突变体构成了一类动物病毒突变体，具有肽链终止突变体预期的特性。
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