The metal-resistant beta-proteobacterium Cupriavidus metallidurans CH34 occurs in metalrich soils overlying Au deposits, and is capable of accumulating highly toxic mobile Au(I/III)-complexes and transforming them into Au(0). In this dissertation a new bacterial detoxification pathway is described that provides a direct link to intracellular Au biomineralization. Copper resistance systems and the cellular redox buffer glutathione seem to be involved. Cellular uptake of highly toxic Au(I/III)-complexes blocks the CupA-dependent Cu(I)-export pathway from the cytoplasm. This results in decreased Au/Cu resistance and accumulation of both metals. Inducible resistance to Au/Cu mixtures involves the periplasmic Cu(I)-oxidase CopA. CopA activity decreases cellular Cu and increases Au contents. As a result, Au(0) nanoparticles could form at the cytoplasmic membrane and in the periplasm. These interactions protect C. metallidurans from mobile Au- and Cu present in auriferous environments, and could explain its capabilities for Au nugget (trans)formation.