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Journal of Bacteriology, July 2001, p. 4357-4363, Vol. 183, No. 14
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.14.4357-4363.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Gene Replacement Analysis of the Butyrolactone Autoregulator Receptor (FarA) Reveals that FarA Acts as a Novel Regulator in Secondary Metabolism of Streptomyces lavendulae FRI-5

Shigeru Kitani,1 Yasuhiro Yamada,2 and Takuya Nihira1,*

Department of Biotechnology, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita, Osaka 565-0871,1 and Department of Applied Biological Science, Faculty of Engineering, Fukuyama University, Fukuyama, Hiroshima 729-0292,2 Japan

Received 7 December 2000/Accepted 25 April 2001

IM-2 [(2R,3R,1'R)-2-1'-hydroxybutyl-3-hydroxymethyl gamma -butanolide] is a gamma -butyrolactone autoregulator which, in Streptomyces lavendulae FRI-5, switches off the production of D-cycloserine but switches on the production of a blue pigment and several nucleoside antibiotics. To clarify the in vivo function of an IM-2-specific receptor (FarA) in the IM-2 signaling cascade of S. lavendulae FRI-5, a farA deletion mutant was constructed by means of homologous recombination. On several solid media, no significant difference in morphology was observed between the wild-type strain and the farA mutant (strain K104), which demonstrated that the IM-2-FarA system does not participate in the morphological control of S. lavendulae FRI-5. In liquid media, the farA mutant overproduced nucleoside antibiotics and produced blue pigment earlier than did the wild-type strain, suggesting that the FarA protein acts primarily as a negative regulator on the biosynthesis of these compounds in the absence of IM-2. However, contrary to the IM-2-dependent suppression of D-cycloserine production in the wild-type strain, overproduction of D-cycloserine was observed in the farA mutant, indicating for the first time that the presence of both IM-2 and intact FarA are necessary for the suppression of D-cycloserine biosynthesis.

* Corresponding author. Mailing address: Department of Biotechnology, Graduate School of Engineering, Osaka University, 2-1 Yamadaoka, Suita, Osaka 565-0871, Japan. Phone: 81-6-6879-7433. Fax: 81-6-6879-7432. E-mail: nihira{at}bio.eng.osaka-u.ac.jp.

Journal of Bacteriology, July 2001, p. 4357-4363, Vol. 183, No. 14
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.14.4357-4363.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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