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J. Biol. Chem., Vol. 281, Issue 5, 2578-2584, February 3, 2006

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A Quantitative Approach to Catabolite Repression in Escherichia coli^*

Katja Bettenbrock¹², Sophia Fischer¹, Andreas Kremling, Knut Jahreis³, Thomas Sauter, and Ernst-Dieter Gilles

From the Systems Biology Group, Max-Planck-Institut für Dynamik komplexer technischer Systeme, 39106 Magdeburg, Germany and AG Genetik, Universität Osnabrück, 49069 Osnabrück, Germany

A dynamic mathematical model was developed to describe the uptake of various carbohydrates (glucose, lactose, glycerol, sucrose, and galactose) in Escherichia coli. For validation a number of isogenic strains with defined mutations were used. By considering metabolic reactions as well as signal transduction processes influencing the relevant pathways, we were able to describe quantitatively the phenomenon of catabolite repression in E. coli. We verified model predictions by measuring time courses of several extra- and intracellular components such as glycolytic intermediates, EII-A^Crr phosphorylation level, both LacZ and PtsG concentrations, and total cAMP concentrations under various growth conditions. The entire data base consists of 18 experiments performed with nine different strains. The model describes the expression of 17 key enzymes, 38 enzymatic reactions, and the dynamic behavior of more than 50 metabolites. The different phenomena affecting the phosphorylation level of EIIA^Crr, the key regulation molecule for inducer exclusion and catabolite repression in enteric bacteria, can now be explained quantitatively.

Received for publication, July 25, 2005 , and in revised form, October 17, 2005.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The on-line version of this article (available at http://www.jbc.org) contains supplements 1 and 2. Supplement 1 contains detailed model documentation, and supplement 2 provides additional information about the modeled units and the experiments used for model validation.

¹ Both authors contributed equally to this work.

³ Supported by the Deutsche Forschungsgemeinschaft through Sonderforschungsbreich 431.

² To whom correspondence should be addressed: Systembiologie, Max-Planck-Institut für Dynamik komplexer technischer Systeme, Sandtorstr. 1, 39106 Magdeburg, Germany. Tel.: 49-391-6110-249; E-mail: bettenbrock{at}mpi-magdeburg.mpg.de.

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