Saito H, Richardson C C
J Virol. 1981 Jan;37(1):343-51. doi: 10.1128/JVI.37.1.343-351.1981.
The product of gene 1.2 of bacteriophage T7 is not required for the growth of T7 in wild-type Escherichia coli since deletion mutants lacking the entire gene 1.2 grow normally (Studier et al., J. Mol. Biol. 135:917-937, 1979). By using a T7 strain lacking gene 1.2, we have isolated a mutant of E. coli that was unable to support the growth of both point and deletion mutants defective in gene 1.2. The mutation, optA1, was located at approximately 3.6 min on the E. coli linkage map in the interval between dapD and tonA; optA1 was 92% cotransducible with dapD. By using the optA1 mutant, we have isolated six gene 1.2 point mutants of T7, all of which mapped between positions 15 and 16 on the T7 genetic map. These mutations have also been characterized by DNA sequence analysis, E. coli optA1 cells infected with T7 gene 1.2 mutants were defective in T7 DNA replication; early RNA and protein synthesis proceeded normally. The defect in T7 DNA replication is manifested by a premature cessation of DNA synthesis and degradation of the newly synthesized DNA. The defect was not observed in E. coli opt+ cells infected with T7 gene 1.2 mutants or in E. coli optA1 cells infected with wild-type T7 phage.
噬菌体T7的基因1.2产物对于T7在野生型大肠杆菌中的生长并非必需,因为缺失整个基因1.2的缺失突变体能够正常生长(Studier等人,《分子生物学杂志》135:917 - 937,1979年)。通过使用缺失基因1.2的T7菌株,我们分离出了一种大肠杆菌突变体,该突变体无法支持基因1.2存在缺陷的点突变体和缺失突变体的生长。该突变,即optA1,位于大肠杆菌连锁图谱上约3.6分钟处,在dapD和tonA之间的区间;optA1与dapD的共转导率为92%。通过使用optA1突变体,我们分离出了六个T7的基因1.2点突变体,所有这些突变体都定位在T7遗传图谱上的15和16位置之间。这些突变也通过DNA序列分析进行了表征,感染T7基因1.2突变体的大肠杆菌optA1细胞在T7 DNA复制方面存在缺陷;早期RNA和蛋白质合成正常进行。T7 DNA复制中的缺陷表现为DNA合成过早停止以及新合成DNA的降解。在感染T7基因1.2突变体的大肠杆菌opt +细胞或感染野生型T7噬菌体的大肠杆菌optA1细胞中未观察到该缺陷。