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Role of copper resistance in Staphylococcus aureus virulence.

Department of Genetics and Genome Biology

About the Project

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.

All bacteria possess mechanisms to resist the toxicity of the essential micronutrient copper. However, our recent publication (Purves et al., 2018) showed that the highly virulent, epidemic, community acquired methicillin resistant Staphylococcus aureus (CA-MRSA) USA300, which shows altered infectivity compared to typical S. aureus, has acquired an additional copper hyper-resistance mechanism.

Our data show that this novel copper resistance locus is uniquely associated with the methicillin resistance element of USA300. This locus confers copper hyper-resistance and is required for S. aureus USA300 intracellular survival within macrophages. 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 other emerging pathogenic isolates and other emerging pathogenic bacteria.

The aim of this project is to further investigate the role of copper resistance mechanisms in the increased infectivity of CA-MRSA.

The student will be part of a lively and friendly interdisciplinary research group and will be trained in a wide range of molecular microbiology techniques including transcriptional analysis, tissue culture, fluorescence and electron microscopy to investigate the impact of additional copper resistance mechanisms on host-pathogen interaction.

Entry requirements

Applicants are required to hold/or expect to obtain a UK Bachelor Degree 2:1 or better in a relevant subject.

The University of Leicester English language requirements apply where applicable:

How to apply

Please refer carefully to the application guidance at

Application enquiries to

Funding Notes

self funded only


1. Purves et al. 2018 A horizontally gene transferred copper resistance locus confers hyper-resistance to antibacterial copper toxicity and enables survival of community acquired methicillin resistant Staphylococcus aureus USA300 in macrophages. Environ Microbiol. 20(4):1576-1589.
2. Zapotoczna et al. 2018. Mobile genetic element-encoded hypertolerance to copper protects Staphylococcus aureus from killing by host phagocytes. (2018) MBio. 9(5). pii: e00550-18.
3. Baker et al., 2011, ‘The Staphylococcus aureus CsoR regulates both chromosomal and plasmid-encoded copper resistance mechanisms,’ Environ. Microbiol. 13:2495-2507.
4. Corbett D, Schuler S, Glenn S, Andrew PW, Cavet JS, Roberts IS. 2011 The combined actions of the copper-responsive repressor CsoR and copper-metallochaperone CopZ modulate CopA-mediated copper efflux in the intracellular pathogen Listeria monocytogenes. Mol Microbiol. Jul;81(2):457-72

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