Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/76211
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Type: Journal article
Title: Phenotypic characterization of a copA mutant of Neisseria gonorrhoeae identifies a link between copper and nitrosative stress
Author: Djoko, K.
Franiek, J.
Edwards, J.
Falsetta, M.
Kidd, S.
Potter, A.
Chen, N.
Apicella, M.
Jennings, M.
McEwan, A.
Citation: Infection and Immunity, 2012; 80(3):1065-1071
Publisher: Amer Soc Microbiology
Issue Date: 2012
ISSN: 0019-9567
1098-5522
Statement of
Responsibility: 
Karrera Y. Djoko, Jessica A. Franiek, Jennifer L. Edwards, Megan L. Falsetta, Stephen P. Kidd, Adam J. Potter, Nathan H. Chen, Michael A. Apicella, Michael P. Jennings and Alastair G. McEwan
Abstract: NGO0579 is annotated copA in the Neisseria gonorrhoeae chromosome, suggesting that it encodes a cation-transporting ATPase specific for copper ions. Compared to wild-type cells, a copA mutant was more sensitive to killing by copper ions but not to other transition metals. The mutant also accumulated a greater amount of copper, consistent with the predicted role of CopA as a copper efflux pump. The copA mutant showed a reduced ability to invade and survive within human cervical epithelial cells, although its ability to form a biofilm on the surface of these cells was not significantly different from that of the wild type. In the presence of copper, the copA mutant exhibited increased sensitivity to killing by nitrite or nitric oxide. Therefore, we concluded that copper ion efflux catalyzed by CopA is linked to the nitrosative stress defense system of Neisseria gonorrhoeae. These observations suggest that copper may exert its effects as an antibacterial agent in the innate immune system via an interaction with reactive nitrogen species.
Keywords: Cells, Cultured; Epithelial Cells; Humans; Neisseria gonorrhoeae; Nitrites; Copper; Nitric Oxide; Bacterial Proteins; Virulence Factors; Virulence; Gene Deletion; Microbial Viability; Stress, Physiological
Rights: Copyright © 2012, American Society for Microbiology. All Rights Reserved.
RMID: 0020117393
DOI: 10.1128/IAI.06163-11
Appears in Collections:Molecular and Biomedical Science publications

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