Brutlag D, Schekman R, Kornberg A
Proc Natl Acad Sci U S A. 1971 Nov;68(11):2826-9. doi: 10.1073/pnas.68.11.2826.
The conversion of single-stranded DNA of bacteriophage M13 to the double-stranded replicative form in Escherichia coli is blocked by rifampicin, an antibiotic that specifically inhibits the host-cell RNA polymerase. Chloramphenicol, an inhibitor of protein synthesis, does not block this conversion. The next stage in phage DNA replication, multiplication of the doublestranded forms, is also inhibited by rifampicin; chloramphenicol, although inhibitory, has a much smaller effect. An E. coli mutant whose RNA polymerase is resistant to rifampicin action does not show inhibition of M13 DNA replication by rifampicin. These findings indicate that a specific rifampicin-RNA polymerase interaction is responsible for blocking new DNA synthesis. It now seems plausible that RNA polymerase has some direct role in the initiation of DNA replication, perhaps by forming a primer RNA that serves for covalent attachment of the deoxyribonucleotide that starts the new DNA chain.
利福平是一种能特异性抑制宿主细胞RNA聚合酶的抗生素,它会阻断噬菌体M13的单链DNA在大肠杆菌中转化为双链复制形式的过程。氯霉素是一种蛋白质合成抑制剂,它不会阻断这种转化。噬菌体DNA复制的下一阶段,即双链形式的增殖,也会受到利福平的抑制;氯霉素虽然有抑制作用,但效果要小得多。一种RNA聚合酶对利福平作用具有抗性的大肠杆菌突变体,不会表现出利福平对M13 DNA复制的抑制作用。这些发现表明,利福平与RNA聚合酶之间的特定相互作用是阻断新DNA合成的原因。现在看来,RNA聚合酶可能在DNA复制起始过程中具有某种直接作用,也许是通过形成一种引物RNA,用于与启动新DNA链的脱氧核糖核苷酸进行共价连接。