Regulation of rRNA transcription is remarkably robust: FIS compensates foraltered nucleoside triphosphate sensing by mutant RNA polymerases at Escherichia coli rrn P1 promoters

We recently identified Escherichia coil RNA polymerase (RNAP) mutants (RNAP beta' Delta 215-220 and beta RH454) that form extremely unstable complexes with rRNA P1 (rm P1) core promoters. The mutant RNAPs reduce transcription and alter growth rate-dependent regulation of rm P1 core promoters, becaus e the mutant RNAPs require higher concentrations of the initiating nucleosi de triphosphate (NTP) for efficient transcription from these promoters than are present in vivo. Nevertheless, the mutants grow almost as well as wild -type cells, suggesting that rRNA synthesis is not greatly perturbed. We re port here that the rrn transcription factor FIS activates the mutant RNAPs more strongly than wild-type RNAP, thereby compensating for the altered pro perties of the mutant RNAPs. FIS activates the mutant RNAPs, at least in pa rt, by reducing the apparent K-ATP for the initiating NTP. This and other r esults suggest that FIS affects a step in transcription initiation after cl osed-complex formation in addition to its stimulatory effect on initial RNA P binding. FIS and NTP levels increase with growth rate, suggesting that ch anging FIS concentrations, in conjunction with changing NTP concentrations, are responsible for growth rate-dependent regulation of rm P1 transcriptio n in the mutant strains. These results provide a dramatic demonstration of the interplay between regulatory mechanisms in rRNA transcription.