Abstract
Copper (Cu) is an essential trace element for all living organisms and used as cofactor in key enzymes of important biological processes, such as aerobic respiration or superoxide dismutation. However, due to its toxicity, cells have developed elaborate mechanisms for Cu homeostasis, which balance Cu supply for cuproprotein biogenesis with the need to remove excess Cu. This review summarizes our current knowledge on bacterial Cu homeostasis with a focus on Gram-negative bacteria and describes the multiple strategies that bacteria use for uptake, storage and export of Cu. We furthermore describe general mechanistic principles that aid the bacterial response to toxic Cu concentrations and illustrate dedicated Cu relay systems that facilitate Cu delivery for cuproenzyme biogenesis. Progress in understanding how bacteria avoid Cu poisoning while maintaining a certain Cu quota for cell proliferation is of particular importance for microbial pathogens because Cu is utilized by the host immune system for attenuating pathogen survival in host cells.
Highlights
30% of all proteins in bacteria depend on metals for their function
Understanding how these potentially toxic metals are imported into bacterial cells and how they are delivered to their target proteins without inducing toxic effects is a crucial issue in metalloprotein biogenesis (Figure 1) [1,2]
The importance of Cu detoxifying systems for bacterial virulence is exemplified by the observation that the inactivation of Cu-exporting P1B -type ATPases in Mycobacterium tuberculosis impairs their ability to proliferate in host macrophages [8,9]
Summary
30% of all proteins in bacteria depend on metals for their function. Understanding how these potentially toxic metals are imported into bacterial cells and how they are delivered to their target proteins without inducing toxic effects is a crucial issue in metalloprotein biogenesis (Figure 1) [1,2]. Cu is located on top of the Irving-Williams series and Cu binding to proteins is usually a thermodynamically favored process [16]. This aids Cu insertion into cuproenzymes, excess Cu could lead to significant mis-metalation of proteins naturally containing. Cu homeostasis and bacterial virulencewith is summarized several recent reviews and thiol:disulfide oxidoreductases covered in depth here [5,10,11,12,13,14,15].[21]
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