Journal
SCIENTIFIC REPORTS
Volume 6, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/srep19602
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Funding
- Royal Society, UK [516002.K5877/ROG]
- Medical Research Council, UK [G0700141]
- Said foundation
- Cambridge Trust
- Biotechnology and Biological Sciences Research Council [BBS/E/J/000C0666, BBS/E/J/000CA538] Funding Source: researchfish
- Medical Research Council [G0700141] Funding Source: researchfish
- BBSRC [BBS/E/J/000C0666, BBS/E/J/000CA538] Funding Source: UKRI
- MRC [G0700141] Funding Source: UKRI
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Vancomycin is a front-line antibiotic used for the treatment of nosocomial infections, particularly those caused by methicillin-resistant Staphylococcus aureus. Despite its clinical importance the global effects of vancomycin exposure on bacterial physiology are poorly understood. In a previous transcriptomic analysis we identified a number of Zur regulon genes which were highly but transiently up-regulated by vancomycin in Streptomyces coelicolor. Here, we show that vancomycin also induces similar zinc homeostasis systems in a range of other bacteria and demonstrate that vancomycin binds to Zn(II) in vitro. This implies that vancomycin treatment sequesters zinc from bacterial cells thereby triggering a Zur-dependent zinc starvation response. The Kd value of the binding between vancomycin and Zn(II) was calculated using a novel fluorometric assay, and NMR was used to identify the binding site. These findings highlight a new biologically relevant aspect of the chemical property of vancomycin as a zinc chelator.
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