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Nucleic Acids Research Advance Access originally published online on September 18, 2006
Nucleic Acids Research 2006 34(17):4960-4967; doi:10.1093/nar/gkl627
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Nucleic Acids Research, 2006, Vol. 34, No. 17 4960-4967
© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Computational Biology

Genetic regulation of fluxes: iron homeostasis of Escherichia coli

Szabolcs Semsey, Anna M. C. Andersson, Sandeep Krishna, Mogens Høgh Jensen, Eric Massé1,* and Kim Sneppen*

Center for Models of Life, Niels Bohr Institute Copenhagen, Denmark 1 Départment de Biochimie, Université de Sherbrooke Sherbrooke, Québec, Canada

*To whom correspondence should be addressed. Tel: +45 353 25352; Fax: +45 353 25425; Email: sneppen{at}nbi.dk

*Corresspondence may also be addressed to Eric Massé. Tel: +1 819 346 1110, ext. 15475; Fax +1 819 564 5340; Email: eric.masse{at}usherbrooke.ca

Received July 7, 2006. Accepted August 10, 2006.

Iron is an essential trace-element for most organisms. However, because high concentration of free intracellular iron is cytotoxic, cells have developed complex regulatory networks that keep free intracellular iron concentration at optimal range, allowing the incorporation of the metal into iron-using enzymes and minimizing damage to the cell. We built a mathematical model of the network that controls iron uptake and usage in the bacterium Escherichia coli to explore the dynamics of iron flow. We simulate the effect of sudden decrease or increase in the extracellular iron level on intracellular iron distribution. Based on the results of simulations we discuss the possible roles of the small RNA RyhB and the Fe–S cluster assembly systems in the optimal redistribution of iron flows. We suggest that Fe–S cluster assembly is crucial to prevent the accumulation of toxic levels of free intracellular iron when the environment suddenly becomes iron rich.


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