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Antibiotic-producing streptomycetes are rich sources of resistance mechanisms against endogenous and exogenous antibiotics. An ECF sigma factor σ R  (SigR) is known to govern the thiol-oxidative stress response in  Streptomyces coelicolor . Amplification of this response is achieved by producing an unstable isoform of σ R  called σ R′ . In this work, we present evidence that antibiotics induce the SigR regulon via a redox-independent pathway, leading to antibiotic resistance. The translation-inhibiting antibiotics enhanced the synthesis of stable σ R , eliciting a prolonged response. WblC/WhiB7, a WhiB-like DNA-binding protein, is responsible for inducing  sigR p1 transcripts encoding the stable σ R . The amount of WblC protein and its binding to the  sigR p1 promoter  in vivo  increased upon antibiotic treatment. A similar phenomenon appears to exist in  Mycobacterium tuberculosis  as well. These findings reveal a novel antibiotic-induced resistance mechanism conserved among actinomycetes, and also give an explicit example of overlap in cellular damage and defense mechanisms between thiol-oxidative and anti- translational stresses.

Induction of a stable sigma factor SigR by translation-inhibiting antibiotics confers resistance to antibiotics