A new Rrf2 repressor family member, SaiR, controls transcription of spxA2 encoding a regulator of the oxidative stress response in Bacillus anthracis.

ABSTRACT: Spx, a member of the ArsC (arsenate reductase) protein family, is highly conserved in Gram-positive bacteria, where it interacts with RNA polymerase to activate transcription in response to toxic oxidants.  In Bacillus anthracis, resistance to oxidative stress requires the activity of two paralogous forms of Spx, SpxA1 and SpxA2.   Suppressor mutations were identified in spxA1 mutant cells that conferred resistance to hydrogen peroxide.  The mutations, which reside in saiR within the operon that also contains the spxA2 gene, caused derepression of spxA2 transcription. The product of saiR is a member of the Rrf2 family of transcriptional repressors.  Derepression of spxA2 in a saiR mutant required SpxA2, indicating an autoregulatory mechanism of spxA2 transcriptional activation.  Reconstruction of SaiR-dependent control of spxA2 was accomplished in Bacillus subtilis, where deletion analysis uncovered two cis-elements within the spxA2 regulatory region that are required for repression.  Both sites bear sequences of dyad symmetry, mutations in which abolished SaiR binding and SaiR-dependent repression of transcription from the spxA2 promoter in vitro.  Previous studies have provided evidence that spxA2 is one of the most highly induced genes in a macrophage infected with B. anthracis.  The work reported herein uncovered a key regulator, SaiR, which controls spxA2 transcriptional activation.

ORGANISM(S): Bacillus anthracis

PROVIDER: GSE57851 | GEO | 2014/05/21

SECONDARY ACCESSION(S): PRJNA248224

REPOSITORIES: GEO