Berget S M, Warner H R, McCorquodale D J
J Virol. 1974 Jul;14(1):78-85. doi: 10.1128/JVI.14.1.78-85.1974.
Two mutants of bacteriophage T5 deficient in the ability to induce wild-type levels of deoxynucleoside monophosphate kinase were isolated and partially characterized. Both mutations were demonstrated to be in a structural gene for the kinase. One of the mutants, designated dnk 10, induces no detectable levels of dCMP, dGMP, or dTMP kinase activity. Because the mutant can successfully infect nonpermissive cells, phage-induced deoxynucleoside monophosphate kinase appears to be an unessential function for phage production. DNA synthesis in dnk 10-infected cells, however, is reduced to 30% of that observed in wild-type-infected cells; phage production is reduced by a comparable amount. The dnk mutation has been mapped and located on the "C" region of the T5 genetic map, 6.3 map units from the C1 locus.
分离出了两种噬菌体T5突变体,它们诱导脱氧核苷单磷酸激酶达到野生型水平的能力存在缺陷,并对其进行了部分特性分析。已证明这两种突变均位于激酶的结构基因中。其中一个突变体命名为dnk 10,它不会诱导出可检测到的dCMP、dGMP或dTMP激酶活性。由于该突变体能成功感染非允许细胞,噬菌体诱导的脱氧核苷单磷酸激酶似乎对噬菌体产生而言并非必需功能。然而,dnk 10感染细胞中的DNA合成减少至野生型感染细胞中观察到的30%;噬菌体产量也相应减少。dnk突变已被定位并位于T5遗传图谱的“C”区域,距离C1位点6.3个图谱单位。