Gold metabolism in Cupriavidus metallidurans
Final Report Abstract
Previous work has shown a strong link between copper and gold metabolism in the metal-resistant bacterium C. metallidurans. In the present project, copper homeostasis, on which gold metabolism relies, was first examined in detail. Responsible are the products of the resistance determinants cup (central product is the Cu(I)-exporting P-type ATPase CupA), cop (periplasmic Cu(I) oxidase CopA), cus (transenvelope efflux pump CusCBA), gig (gold induced genes, function unclear) and glutathione (GSH). Full copper resistance requires the interaction of these systems. The absence of Cup results in the highest loss of resistance in all mutants. As important as the Cup system was, it could not provide full resistance alone. This required the other systems, especially Cop and Cus, with smaller contributions from Gig and GSH. Based on this knowledge of copper resistance, it has now been discovered that different Au(III) tetrachloride solutions differ significantly in their effects on cells. In general, Au ions are not stable in H2O because they have a more positive redox potential and therefore can oxidize H2O, creating metallic gold. However, meta-stability can be achieved by Au complexes, for example Au(III)Cl4-. The four bulky Cl ions surround the Au(III) central atom and shielding it from H2O. If Au(III)Cl4- is produced by oxidizing Au(0) in aqua regia, the stock solution is stable for months, but turns slowly purple due to the formation of colloidal Au(0), which ultimately precipitates as brown complexes. Upon contact with C. metallidurans, this solution is oxidized to Au(I) so slowly in the periplasm that CopA can oxidize the Au(I) and thus both limits its uptake into the cell and enables its permanent disposal as gold nanoparticles. However, if Au(III)Cl4- is produced by oxidizing Au(0) with chlorine gas, then it is stabilized in the stock solution by the Cl2 that is still present. But upon contact with the reduced cellular components in the periplasm, Au(I) is formed so quickly that 20-times more gold reaches the cell interior than in case of aqua regia gold. In addition, the periplasmic Au(I) inhibits all Cu(I)- dependent physiological processes in this compartment. This involves also the metalation of CopA by copper, whereby CopA does not achieve its full activity and cannot oxidize Au(I). This clearly demonstrated that the chemical environment of Au(III)Cl4- influences its metastability, subsequently its interaction with C. metallidurans, the formation of periplasmic gold nanoparticles and also the geomicrobiological formation of secondary gold nuggets. Further results of the project concerned the general molecular processes of multiple metal homeostasis and the way in which periplasmic Cu(I) can become regulatory active.
Publications
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"Full copper resistance in Cupriavidus metallidurans requires the interplay of many resistance systems" Appl Environ Microbiol 89
Hirth, N., M. S. Gerlach, N. Wiesemann, M. Herzberg, C. Grosse & D. H. Nies
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The Sensory Histidine Kinase CusS of Escherichia coli Senses Periplasmic Copper Ions. Microbiology Spectrum, 11(2).
Rismondo, Jeanine; Große, Cornelia & Nies, Dietrich H.
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"A gold speciation that adds a second layer to synergistic gold-copper toxicity in Cupriavidus metallidurans" Appl Environ Microbiol 90
Hirth, N., N. Wiesemann, S. Krüger, M. S. Gerlach, K. Preußner, D. Galea, M. Herzberg, C. Große & D. H. Nies
