Participation of Rho-dependent transcription termination in oxidative stress sensitivity caused by an rpoB mutation.

The role of transcription termination process for gene expression regulation is poorly understood. Either a multicopy supply of the rof gene or bicyclomycin, both of which inhibit the transcription termination Rho factor, suppressed the increased sensitivity to oxidative stress of the rifampicin-resistant rpoB mutation in Escherichia coli. Multi-copy supply of the rnk gene also suppressed oxidative stress sensitivity, coincident with the recovery of the reduced concentration of nucleoside triphosphates in the mutant cells, which is one of the factors that affects transcription termination efficiency in vitro. Thus, an appropriate, nonexcessive termination frequency at Rho-dependent transcription terminators might contribute to oxidative stress survival. Clinical application of oxidative stress against drug resistant bacteria is also discussed.