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Substrate induction and glucose repression of maltose utilization by Streptomyces coelicolor A3(2) is controlled by malR, a member of the lacI-galR family of regulatory genes

Van Wezel, G.P., White, J., Young, J.P.W., Postma, P.W. and Bibb, M.J. (1997) Substrate induction and glucose repression of maltose utilization by Streptomyces coelicolor A3(2) is controlled by malR, a member of the lacI-galR family of regulatory genes. Molecular Microbiology. pp. 537-549. ISSN 0950-382X

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Abstract

malR of Strepomyces coelicolor A3(2) encodes a homologue of the Lacl/Galr family of repressor proteins, and is divergently transcribed from the malEFG gene cluster, which encodes components of an ATP-dependent transport system that is required for maltose utilization. Transcription of malE was induced by maltose and repressed by glucose. Disruption or deletion of malR resulted in constitutive, glucose-insensitive malE transcription at a level markedly above that observed in the parental malR+ strain, and overproduction of MalR prevented growth on maltose as carbon source. Consequently, MalR plays a crucial role in both substrate induction and glucose repression of maltose utilization. MalR is expressed from a single promoter with transcription initiating at the first G of the predicted GTG translataion start codon.

Item Type: Article
Copyright, Publisher and Additional Information: © 1997 Blackwell Science Ltd. This is an electronic version of an article published in Molecular Microbiology: complete citation information for the final version of the paper, as published in the print edition of Molecular Microbiology, is available on the Blackwell Synergy online delivery service, accessible via the journal's website at http://www.blackwellpublishing.com/journal.asp?ref=0950-382X or www.blackwell-synergy.com
Academic Units: The University of York > Biology (York)
Depositing User: Peter Young
Date Deposited: 22 Apr 2005
Last Modified: 17 Oct 2013 14:42
Status: Published
Refereed: Yes
Related URLs:
URI: http://eprints.whiterose.ac.uk/id/eprint/408

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