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Trace Metals and Infectious Diseases$
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Jerome O. Nriagu and Eric P. Skaar

Print publication date: 2015

Print ISBN-13: 9780262029193

Published to MIT Press Scholarship Online: May 2016

DOI: 10.7551/mitpress/9780262029193.001.0001

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Common Mechanisms of Bacterial Metal Homeostasis

Common Mechanisms of Bacterial Metal Homeostasis

Chapter:
(p.57) 5 Common Mechanisms of Bacterial Metal Homeostasis
Source:
Trace Metals and Infectious Diseases
Author(s):

James A. Imlay

Publisher:
The MIT Press
DOI:10.7551/mitpress/9780262029193.003.0005

Transition metals are required for the function of nearly half the enzymatic machinery of organisms. Metals compete for enzyme-binding sites and inappropriate metallation inhibits enzyme function. Thus microbes work hard to acquire, balance, and sort their metal pools. This chapter surveys common tactics by which bacteria control intracellular iron, manganese, copper, and zinc. Focus is on Escherichia coli, for which enough information is available to attempt an integrated view. High-affinity import systems are regulated at the level of transcription by specific metal-sensing transcription factors. If these importers are insufficient, then metal-sparing strategies are engaged for iron and zinc, the two metals needed to activate essential enzymes. At the other extreme, metal overload can result in chemical injuries (Fe, Zn, Cu) and the mismetallation of noncognate enzymes (Fe, Zn, Mn). Export systems are induced to avoid these outcomes. Cu movement may sometimes be chaperone driven, but other metals may reversibly sample protein-binding sites and populate them according to the relative binding strengths of proteins and competing metabolite ligands. Thus metal pool sizes must be controlled and balanced.

Keywords:   metal availability, metal acquisition, metal control, Escherichia coli, metal overload

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