The ActSR two-component regulatory system is a member of a homologous group of global redox-responsive regulatory systems that adjust the expression of energy-consuming and energy-supplying metabolic pathways in order to maintain cellular redox balance. In this study, the transcriptional organization of the locus was determined and the effect of system inactivation on stress resistance was investigated. It was found that is transcribed as a monocistronic mRNA and is transcribed along with as a bicistronic mRNA, while is also transcribed as a monocistronic message. Each message is initiated from a separate promoter. Inactivation of resulted in decreased resistance to membrane stress (sodium dodecyl sulfate), acid stress (pH 5.5), iron starvation (bipyridyl) and iron excess (FeCl), and antibiotic stress (tetracycline and ciprofloxacin). Resistance to oxidative stress in the form of organic peroxide (cumene hydroperoxide) increased, while resistance to inorganic peroxide (HO) decreased. An insertion mutant displayed reduced catalase activity, even though transcription of and remained unchanged. Complementation of the inactivation mutant with plasmid-encoded or overexpression of , encoding ferrochelatase, restored wild-type catalase activity and HO resistance levels. Gel mobility shift and promoter fusion results indicated that ActR is a positive regulator of that binds directly to the promoter region. Thus, inactivation of the ActSR system affects resistance to multiple stresses, including reduced resistance to HO resulting from a reduction in catalase activity due to reduced expression of .
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