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Journal of Bacteriology, December 2004, p. 8490-8498, Vol. 186, No. 24
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.24.8490-8498.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Regulation of {sigma}B by an Anti- and an Anti-Anti-Sigma Factor in Streptomyces coelicolor in Response to Osmotic Stress

Eun-Jin Lee,1 You-Hee Cho,2 Hyo-Sub Kim,1 Bo-Eun Ahn,1 and Jung-Hye Roe1*

School of Biological Sciences and Institute of Microbiology, Seoul National University,1 Department of Life Science, Sogang University, Seoul, Korea2

Received 26 April 2004/ Accepted 25 August 2004

{sigma}B, a homolog of stress-responsive {sigma}B 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 {sigma}B and prevented {sigma}B-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 {sigma}B 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 {sigma}B-dependent manner. It antagonized the inhibitory action of RsbA on {sigma}B-directed transcription and was phosphorylated by RsbA in vitro. These results support the hypothesis that the rapid induction of {sigma}B target genes by osmotic stress results from modulation of {sigma}B 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 {sigma}B and its inhibitor antagonist.

* Corresponding author. Mailing address: School of Biological Sciences and Institute of Microbiology, Seoul National University, Seoul 151-742, Korea. Phone: 82 2 880 6706. E-mail: jhroe{at}plaza.snu.ac.kr.

Journal of Bacteriology, December 2004, p. 8490-8498, Vol. 186, No. 24
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.24.8490-8498.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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