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Fe-S cluster metabolism as a target for Cobalt


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The findings of the researchers at the Laboratory of Metals in Chemistry and Biology support the hypothesis that cobalt inhibits the biosynthesis and/or repair of Fe-S clusters by competing directly with iron, and illustrate the importance of iron-sulphur cluster biogenesis in cells.​​

Published on 10 October 2007
Using the bacterium Escherichia coli as a model, the Biocatalysis team at the Laboratory of Metals in Chemistry and Biology is working to identify potential targets of and the molecular mechanisms underpinning cobalt toxicity.

Working alongside a bacterial microbiology team from the CNRS unit in Marseille (UPR-CNRS 9043), the Biocatalysis team has demonstrated in vivo cobalt deactivation inactivation of a number of essential iron-sulfphur cluster proteins. Cobalt tolerance requires the involvement of proteins belonging to the SUF system, the iron-sulfphur cluster biosynthetic mechanism that is particularly active under conditions of stress (oxidative stress or iron deficiency). In vitro studies have also revealed that cobalt does not react directly with previously assembled iron-sulfphur clusters, but rather with the labile iron-sulfphur clusters found in the scaffold proteins involved in iron-sulfphur cluster biosynthesis.

These findings support the hypothesis that cobalt inhibits the biosynthesis and/or repair of iron-sulfphur clusters by competing directly with iron at the relevant sites.
 
 

The results of this research, which was carried out under the ToNuc-E programme, illustrate the key role of iron-sulfphur cluster biogenesis within cells.

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