Hobbs L J, Nossal N G
Laboratory of Molecular and Cellular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892-0830, USA.
J Bacteriol. 1996 Dec;178(23):6772-7. doi: 10.1128/jb.178.23.6772-6777.1996.
Bacteriophage T4 rnh encodes an RNase H that removes ribopentamer primers from nascent DNA chains during synthesis by the T4 multienzyme replication system in vitro (H. C. Hollingsworth and N. G. Nossal, J. Biol. Chem. 266:1888-1897, 1991). This paper demonstrates that either T4 RNase HI or Escherichia coli DNA polymerase I (Pol I) is essential for phage replication. Wild-type T4 phage production was not diminished by the polA12 mutation, which disrupts coordination between the polymerase and the 5'-to-3' nuclease activities of E. coli DNA Pol I, or by an interruption in the gene for E. coli RNase HI. Deleting the C-terminal amino acids 118 to 305 from T4 RNase H reduced phage production to 47% of that of wild-type T4 on a wild-type E. coli host, 10% on an isogenic host defective in RNase H, and less than 0.1% on a polA12 host. The T4 rnh(delta118-305) mutant synthesized DNA at about half the rate of wild-type T4 in the polA12 host. More than 50% of pulse-labelled mutant DNA was in short chains characteristic of Okazaki fragments. Phage production was restored in the nonpermissive host by providing the T4 rnh gene on a plasmid. Thus, T4 RNase H was sufficient to sustain the high rate of T4 DNA synthesis, but E. coli RNase HI and the 5'-to-3' exonuclease of Pol I could substitute to some extent for the T4 enzyme. However, replication was less accurate in the absence of the T4 RNase H, as judged by the increased frequency of acriflavine-resistant mutations after infection of a wild-type host with the T4 rnh (delta118-305) mutant.
噬菌体T4的rnh基因编码一种核糖核酸酶H,在体外由T4多酶复制系统合成过程中,该酶可从新生DNA链上去除核糖五聚体引物(H. C. 霍林斯沃思和N. G. 诺萨尔,《生物化学杂志》266:1888 - 1897,1991)。本文证明,T4核糖核酸酶HI或大肠杆菌DNA聚合酶I(Pol I)对噬菌体复制至关重要。野生型T4噬菌体的产生不受polA12突变的影响,该突变破坏了大肠杆菌DNA Pol I的聚合酶和5'至3'核酸酶活性之间的协调,也不受大肠杆菌核糖核酸酶HI基因中断的影响。从T4核糖核酸酶H中删除C末端氨基酸118至305,在野生型大肠杆菌宿主上,噬菌体产量降至野生型T4的47%;在核糖核酸酶H缺陷的同基因宿主上,降至10%;在polA12宿主上,降至不到0.1%。T4 rnh(delta118 - 305)突变体在polA12宿主中合成DNA的速度约为野生型T4的一半。超过50%的脉冲标记突变体DNA存在于冈崎片段特有的短链中。通过在质粒上提供T4 rnh基因,噬菌体产量在非允许宿主中得以恢复。因此,T4核糖核酸酶H足以维持T4 DNA的高速合成,但大肠杆菌核糖核酸酶HI和Pol I的5'至3'外切核酸酶可以在一定程度上替代T4酶。然而,根据用T4 rnh(delta118 - 305)突变体感染野生型宿主后吖啶黄素抗性突变频率增加来判断,在没有T4核糖核酸酶H的情况下,复制的准确性较低。