Dysregulation of transition metal ion homeostasis is the molecular basis for cadmium toxicity in Streptococcus pneumoniae

Stephanie L. Begg, Bart A. Eijkelkamp, Zhenyao Luo, Rafael M. Couñago, Jacqueline R. Morey, Megan J. Maher, Cheryl-lynn Y. Ong, Alastair G. McEwan, Bostjan Kobe, Megan L. O’Mara, James C. Paton and Christopher A. McDevitt ()
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Stephanie L. Begg: Research Centre for Infectious Diseases, School of Biological Sciences, The University of Adelaide
Bart A. Eijkelkamp: Research Centre for Infectious Diseases, School of Biological Sciences, The University of Adelaide
Zhenyao Luo: School of Chemistry and Molecular Biosciences, University of Queensland
Rafael M. Couñago: School of Chemistry and Molecular Biosciences, University of Queensland
Jacqueline R. Morey: Research Centre for Infectious Diseases, School of Biological Sciences, The University of Adelaide
Megan J. Maher: La Trobe Institute for Molecular Science, La Trobe University
Cheryl-lynn Y. Ong: School of Chemistry and Molecular Biosciences, University of Queensland
Alastair G. McEwan: School of Chemistry and Molecular Biosciences, University of Queensland
Bostjan Kobe: School of Chemistry and Molecular Biosciences, University of Queensland
Megan L. O’Mara: School of Chemistry and Molecular Biosciences, University of Queensland
James C. Paton: Research Centre for Infectious Diseases, School of Biological Sciences, The University of Adelaide
Christopher A. McDevitt: Research Centre for Infectious Diseases, School of Biological Sciences, The University of Adelaide

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: Abstract Cadmium is a transition metal ion that is highly toxic in biological systems. Although relatively rare in the Earth’s crust, anthropogenic release of cadmium since industrialization has increased biogeochemical cycling and the abundance of the ion in the biosphere. Despite this, the molecular basis of its toxicity remains unclear. Here we combine metal-accumulation assays, high-resolution structural data and biochemical analyses to show that cadmium toxicity, in Streptococcus pneumoniae, occurs via perturbation of first row transition metal ion homeostasis. We show that cadmium uptake reduces the millimolar cellular accumulation of manganese and zinc, and thereby increases sensitivity to oxidative stress. Despite this, high cellular concentrations of cadmium (~17 mM) are tolerated, with negligible impact on growth or sensitivity to oxidative stress, when manganese and glutathione are abundant. Collectively, this work provides insight into the molecular basis of cadmium toxicity in prokaryotes, and the connection between cadmium accumulation and oxidative stress.

Date: 2015
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DOI: 10.1038/ncomms7418

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