How Bacteria Handle Copper

Abstract

Copper in biological systems presents a formidable problem: it is essential for life, yet highly reactive and a potential source of cell damage. Tight control of copper is thus a cellular necessity. To meet this challenge, cells have evolved pumps for transmembranous transport, chaperones for intracellular routing, oxidases and reductases to change the oxidation state of copper, and regulators to control gene expression in response to copper. These systems are complemented by specific mechanisms for the insertion of copper into enzymes. Copper homeostasis has evolved early in evolution and some components have been conserved from bacteria to humans. This has allowed researchers to apply knowledge across phyla and even involving human copper homeostatic diseases to elucidate the fundamental mechanism of cellular copper homeostasis. After an introduction to the properties of copper and its role in biological systems, some of the best studied bacterial systems for copper homeostasis will be discussed.

Influence of Copper Resistance Determinants on Gold Transformation by Cupriavidus metallidurans Strain CH34

“…This suggests that organisms living in metal-rich environments are likely to encounter toxic effects from mobile copper rather than from mobile gold complexes. This is well reflected in genetic make-up of these bacteria, which harbor specific copper resistance systems used to regulate copper homeostasis (16). In contrast, toxic concentrations of gold complexes might rarely be encountered; thus, specific genetic gold resistance systems are likely to be energetically unfavorable, if other, e.g., copper, metal resistance, and homeostasis systems can be coutilized.…”

“…Bacterial copper homeostasis has been studied in several bacteria (16,17). Common motifs include (i) the export of surplus copper from the cytoplasm by P IB1 -type ATPases (TC 3.A.3) (18-21), often regulated at the level of transcription by MerR-type regulatory proteins such as CueR (22), (ii) cytoplasmic and periplasmic copper chaperones, (iii) the transport of copper ions to the outside of the cell by RND-driven (TC 2.A.6, resistance-nodulation-cell division protein family) transenvelope efflux complexes such as CusCBA (23)(24)(25)(26) that are regulated by two-component regulatory systems (27), and (iv) oxidation of Cu(I) to Cu(II) in the periplasm.…”

Geobiological Cycling of Gold: From Fundamental Process Understanding to Exploration Solutions

“…This suggests that organisms living in metal-rich environments are likely to encounter toxic effects from mobile copper rather than from mobile gold complexes. This is well reflected in genetic make-up of these bacteria, which harbor specific copper resistance systems used to regulate copper homeostasis [56]. In contrast, toxic concentrations of gold complexes might rarely be encountered; hence specific genetic gold resistance systems are likely to be energetically unfavorable, if other copper resistance and homeostasis systems can be co-utilized.…”

Non-enzymic copper reduction by menaquinone enhances copper toxicity in Lactococcus lactis IL1403

“…Examples are cytochrome oxidases involved in respiration or superoxide dismutases, which are essential to combat oxidative stress (Karlin, 1993). Oxidative stress can be caused by copper ions which participate in Fenton-type reactions and thereby generate reactive oxygen species (Magnani & Solioz, 2007). Copper ions can also damage [Fe-S]-cluster proteins by displacing the iron (Macomber & Imlay, 2009).…”

“…Inside the cell, specialized proteins are responsible for copper handling, such as insertion into cuproenzymes or delivery to copper-responsive regulators [for recent reviews, see Solioz et al (2010) and Magnani & Solioz (2007)]. To the extent it has been studied, these copper homeostatic proteins bind Cu + and it is generally assumed that Cu + prevails in the reducing environment of the cytoplasm, without the need for a copper reductase (Solioz et al, 2011).…”