Proc Natl Acad Sci U S A 68: 2826-9 (1971)
The conversion of single-stranded I)NA 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 double-stranded 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.
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