Lookup NU author(s): Dr Emma Tarrant,
Dr Kevin Waldron
This work is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0).
© 2018 Society for Applied Microbiology and John Wiley & Sons Ltd. Excess copper is highly toxic and forms part of the host innate immune system's antibacterial arsenal, accumulating at sites of infection and acting within macrophages to kill engulfed pathogens. We show for the first time that a novel, horizontally gene transferred copper resistance locus (copXL), uniquely associated with the SCCmec elements of the highly virulent, epidemic, community acquired methicillin resistant Staphylococcus aureus (CA-MRSA) USA300, confers copper hyper-resistance. These genes are additional to existing core genome copper resistance mechanisms, and are not found in typical S. aureus lineages, but are increasingly identified in emerging pathogenic isolates. Our data show that CopX, a putative P1B-3-ATPase efflux transporter, and CopL, a novel lipoprotein, confer copper hyper-resistance compared to typical S. aureus strains. The copXL genes form an operon that is tightly repressed in low copper environments by the copper regulator CsoR. Significantly, CopX and CopL are important for S. aureus USA300 intracellular survival within macrophages. Therefore, the emergence of new S. aureus clones with the copXL locus has significant implications for public health because these genes confer increased resistance to antibacterial copper toxicity, enhancing bacterial fitness by altering S. aureus interaction with innate immunity.
Author(s): Purves J, Thomas J, Riboldi GP, Zapotoczna M, Tarrant E, Andrew PW, Londono A, Planet PJ, Geoghegan JA, Waldron KJ, Morrissey JA
Publication type: Article
Publication status: Published
Journal: Environmental Microbiology
Print publication date: 01/04/2018
Online publication date: 26/03/2018
Acceptance date: 27/02/2018
Date deposited: 10/04/2018
ISSN (print): 1462-2912
ISSN (electronic): 1462-2920
Publisher: Blackwell Publishing Ltd
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