There is growing interest in utilizing copper for infection control owing to its antibacterial properties (Noyce et al., 2006 Warnes et al., 2012 Lemire et al., 2013). Excess copper, however, is also cytotoxic. Since patterns of copper response are conserved through the Proteobacteria, we propose a cell-wide view of copper detoxification and copper tolerance that can be used to identify novel targets for copper-based antibacterial therapeutics.Ĭopper is an essential micronutrient for bacteria, serving as an electron carrier and redox catalyst in various cuproenzymes (Rensing and Grass, 2003 Andreini et al., 2008 Festa and Thiele, 2011 Vest et al., 2013). Tapping into the abundant research data on two key organisms, Escherichia coli and Salmonella enterica, we show that copper resistance requires both the direct copper homeostatic response and also the indirect accessory pathways that deal with copper-induced damage. In this review, we summarize the bacterial cell-wide response to copper toxicity in Enterobacteria. To evade copper toxicity, bacteria not only control intracellular copper homeostasis, but they must also repair the damage caused by excess copper. Yet, excess copper is extremely toxic, and is exploited as a bacteriocide in medical and biotechnological applications and also by the mammalian immune system. Copper is a required micronutrient for bacteria and an essential cofactor for redox-active cuproenzymes.
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