EFFECT OF STREPTOVARICIN ON RNA SYNTHESIS IN PHAGE T4-INFECTED ESCHERICHIA COLI

As reported in our previous papers (Mizuno et al., 1968a; Mizuno et al., 1968b; Umezawa et al., 1968; Nitta et al., 1968), streptovaricin, rifamycins and rifampicin, which have structures resembling one another, inhibit initiation of RNA synthesis in E. coli, presumably binding to the RNA polymerase, but do not inhibit the RNA synthesis by RNA polymerase obtained from a resistant mutant of E. coli. Hartmann et al. (1967) also reported a similar observation on inhibition of RNA polymerase by rifamycins. Recently, it was proved by Wehrli et al. (1968) that E. coli RNA polymerase forms a stable complex with rifampicin but the enzyme obtained from a rifampicin-resistant mutant of E. coli does not form such a complex with the antibiotic. Genetic analysis made by Yura and Igarashi (1969) suggested that the RNA polymerase in streptovaricin-resistant mutants of E. coli would be structurally modified. These findings indicate that these antibiotics might be useful to study the role of E. coli RNA polymerase in transcription of phage genes in bacteriophage-infected E. coli. We will report in the present communication the effect of streptovaricin (SV) on pulse labeled RNA synthesis in SV-sensitive and resistant E. coli at various times after phage T4-infection. The results obtained indicate that phage RNA synthesis in SV-sensitive E. coli is inhibited by SV at any time after infection, but that in SV-resistant cells it is not inhibited at any time. © 1969.