Open AccessRegulation of σ B by an Anti- and an Anti-Anti-Sigma Factor in Streptomyces coelicolor in Response to Osmotic Stress
Author(s) -
Eun Jin Lee,
YouHee Cho,
Hyo Sub Kim,
Bo Eun Ahn,
Jung Hye Roe
Publication year - 2004
Publication title -
journal of bacteriology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.652
H-Index - 246
eISSN - 1067-8832
pISSN - 0021-9193
DOI - 10.1128/jb.186.24.8490-8498.2004
Subject(s) - streptomyces coelicolor , biology , sigma factor , osmotic shock , sigma , streptomyces , actinomycetales , microbiology and biotechnology , bacterial protein , genetics , bacteria , physics , gene , promoter , gene expression , quantum mechanics
sigmaB, a homolog of stress-responsive sigmaB of Bacillus subtilis, controls both osmoprotection and differentiation in Streptomyces coelicolor A3 (2). Its gene is preceded by rsbA and rsbB genes encoding homologs of an anti-sigma factor, RsbW, and its antagonist, RsbV, of B. subtilis, respectively. Purified RsbA bound to sigmaB and prevented sigmaB-directed transcription from the sigBp1 promoter in vitro. An rsbA-null mutant exhibited contrasting behavior to the sigB mutant, with elevated sigBp1 transcription, no actinorhodin production, and precocious aerial mycelial formation, reflecting enhanced activity of sigmaB in vivo. Despite sequence similarity to RsbV, RsbB lacks the conserved phosphorylatable serine residue and its gene disruption produced no distinct phenotype. RsbV (SCO7325) from a putative six-gene operon (rsbV-rsbR-rsbS-rsbT-rsbU1-rsbU) was strongly induced by osmotic stress in a sigmaB-dependent manner. It antagonized the inhibitory action of RsbA on sigmaB-directed transcription and was phosphorylated by RsbA in vitro. These results support the hypothesis that the rapid induction of sigmaB target genes by osmotic stress results from modulation of sigmaB activity by the kinase-anti-sigma factor RsbA and its phosphorylatable antagonist RsbV, which function by a partner-switching mechanism. Amplified induction could result from a rapid increase in the synthesis of both sigmaB and its inhibitor antagonist.