The soxRS regulon orchestrates a multifaceted defense against oxidative str
ess, by inducing the transcription of similar to 15 genes. The induction of
this regulon by redox agents, known to mediate O radical anion production,
led to the view that O2 radical anion is one signal to which it responds.
However, redox cycling agents deplete cellular reductants while producing O
2 radical anion, and one may question whether the regulon responds to the d
epletion of some cytoplasmic reductant or to O2 radical anion, or both. We
demonstrate that raising [O2 radical anion] by mutational deletion of super
oxide dismutases and/or by addition of paraquat, both under aerobic conditi
ons, causes induction of a member of the soxRS regulon and that a mutationa
l defect in soxRS eliminates that induction. This establishes that O2 radic
al anion, directly or indirectly, can cause induction of this defensive reg
ulon.