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Journal of Bacteriology, July 2006, p. 5014-5023, Vol. 188, No. 14
0021-9193/06/$08.00+0     doi:10.1128/JB.00307-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

DevA, a GntR-Like Transcriptional Regulator Required for Development in Streptomyces coelicolor

Paul A. Hoskisson,1*,{dagger} Sebastien Rigali,2 Kay Fowler,1 Kim C. Findlay,1 and Mark J. Buttner1

John Innes Centre, Norwich Research Park, Colney Lane, Norwich, NR4 7UH, United Kingdom,1 Centre d'Ingeniere des Proteins, Universite de Liege, Institute de Chimie B6, Sart-Tilman, B-4000, Liege, Belgium2

Received 2 March 2006/ Accepted 20 April 2006

The gram-positive filamentous bacterium Streptomyces coelicolor has a complex developmental cycle with three distinct phases: growth of the substrate mycelium, development of reproductive structures called aerial hyphae, and differentiation of these aerial filaments into long chains of exospores. During a transposon mutagenesis screen, we identified a novel gene (devA) required for proper development. The devA mutant produced only rare aerial hyphae, and those that were produced developed aberrant spore chains that were much shorter than wild-type chains and had misplaced septa. devA encodes a member of the GntR superfamily, a class of transcriptional regulators that typically respond to metabolite effector molecules. devA forms an operon with the downstream gene devB, which encodes a putative hydrolase that is also required for aerial mycelium formation on R5 medium. S1 nuclease protection analysis showed that transcription from the single devA promoter was temporally associated with vegetative growth, and enhanced green fluorescent protein transcriptional fusions showed that transcription was spatially confined to the substrate hyphae in the wild type. In contrast, devAB transcript levels were dramatically upregulated in a devA mutant and the devA promoter was also active in aerial hyphae and spores in this background, suggesting that DevA might negatively regulate its own production. This suggestion was confirmed by gel mobility shift assays that showed that DevA binds its own promoter region in vitro.


* Corresponding author. Mailing address: Department of Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom. Phone: (44) (0)1224 555761. Fax: (44) (0)1224 555844. E-mail: p.hoskisson{at}abdn.ac.uk.

{dagger} Present address: Department of Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, United Kingdom.


Journal of Bacteriology, July 2006, p. 5014-5023, Vol. 188, No. 14
0021-9193/06/$08.00+0     doi:10.1128/JB.00307-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




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