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Regulation of D-xylose metabolism in Caulobacter crescentus by a LacI-type repressor

Stephens, C. and Christen, B. and Watanabe, K. and Fuchs, T. and Jenal, U.. (2007) Regulation of D-xylose metabolism in Caulobacter crescentus by a LacI-type repressor. Journal of bacteriology, Vol. 189, H. 24. pp. 8828-8834.

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Official URL: http://edoc.unibas.ch/dok/A5258539

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Abstract

In the oligotrophic freshwater bacterium Caulobacter crescentus, D-xylose induces expression of over 50 genes, including the xyl operon, which encodes key enzymes for xylose metabolism. The promoter (P(xylX)) controlling expression of the xyl operon is widely used as a tool for inducible heterologous gene expression in C. crescentus. We show here that P(xylX) and at least one other promoter in the xylose regulon (P(xylE)) are controlled by the CC3065 (xylR) gene product, a LacI-type repressor. Electrophoretic gel mobility shift assays showed that operator binding by XylR is greatly reduced in the presence of D-xylose. The data support the hypothesis that there is a simple regulatory mechanism in which XylR obstructs xylose-inducible promoters in the absence of the sugar; the repressor is induced to release DNA upon binding D-xylose, thereby freeing the promoter for productive interaction with RNA polymerase. XylR also has an effect on glucose metabolism, as xylR mutants exhibit reduced expression of the Entner-Doudoroff operon and their ability to utilize glucose as a sole carbon and energy source is compromised.
Faculties and Departments:05 Faculty of Science > Departement Biozentrum > Infection Biology > Molecular Microbiology (Jenal)
05 Faculty of Science > Departement Biozentrum > Growth & Development > Molecular Microbiology (Jenal)
UniBasel Contributors:Jenal, Urs
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:American Society for Microbiology
ISSN:1098-5530
Note:Publication type according to Uni Basel Research Database: Journal article
Last Modified:22 Mar 2012 14:20
Deposited On:22 Mar 2012 13:20

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