Inhibition by lipiarmycin of bacteriophage growth in Bacillus subtilis

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Abstract
Lipiarmycin, a specific inhibitor of initiation of transcription, was used to study the role of host RNA polymerase in the transcription programs of various phages of B. subtilis. Unlike rifampin, lipiarmycin preferentially inhibits transcription dependent on the .sigma. subunit of RNA polymerase because it inactivates holoenzyme at a much greater rate than it does core enzyme. With phage SPO1, addition of lipiarmycin at a middle-to-late time of infection did not inhibit phage production even though phage production was sensitive to addition of rifampin at that time. Unmodified host RNA polymerase holoenzyme apparently becomes dispensable after transcription of early classes of SPO1 genes, even though host core enzyme is required for synthesis of all classes of phage RNA. SPO1-modified forms of RNA polymerase, which lack .sigma. subunit but contain phage-coded polypeptides and are able to transcribe middle and late genes, were resistant to lipiarmycin in vitro. For phage .vphi. 105, phage development was insensitive to both lipiarmycin and rifampin in wild-type cells and resistant to both drugs in resistant mutant cells, leading to the conclusion that the activity of host holoenzyme was required for phage RNA synthesis. Growth of phage PBS2, which was resistant to rifampin, was sensitive to the addition of lipiarmycin at early times of infection of a wild-type host strain. In a lipiarmycin-resistant mutant host, PBS2 growth was resistant to lipiarmycin. Host holoenzyme apparently plays a previously unanticipated role in transcription of PBS2 genes.