- For Vibrio cholerae, the coordinated import and export of Na+ is crucial for adaptation to habitats with different osmolarities. We investigated the Na+-extruding branch of the sodium cycle in this human pathogen by in vivo Na-23-NMR spectroscopy. The Na+ extrusion activity of cells was monitored after adding glucose which stimulated respiration via the Na+-translocating NADH:quinone oxidoreductase (Na+-NQR). In a V. cholerae deletion mutant devoid of the Na+-NQR encoding genes (nqrA-F), rates of respiratory Na+ extrusion were decreased by a factor of four, but the cytoplasmic Na+ concentration was essentially unchanged. Furthermore, the mutant was impaired in formation of transmembrane voltage (Delta psi, inside negative) and did not grow under hypoosmotic conditions at pH 8.2 or above. This growth defect could be complemented by transformation with the plasmid encoded nqr operon. In an alkaline environment, Na+/H+ antiporters acidify the cytoplasm at the expense of the transmembrane voltage. It is proposed that, at alkaline pH andFor Vibrio cholerae, the coordinated import and export of Na+ is crucial for adaptation to habitats with different osmolarities. We investigated the Na+-extruding branch of the sodium cycle in this human pathogen by in vivo Na-23-NMR spectroscopy. The Na+ extrusion activity of cells was monitored after adding glucose which stimulated respiration via the Na+-translocating NADH:quinone oxidoreductase (Na+-NQR). In a V. cholerae deletion mutant devoid of the Na+-NQR encoding genes (nqrA-F), rates of respiratory Na+ extrusion were decreased by a factor of four, but the cytoplasmic Na+ concentration was essentially unchanged. Furthermore, the mutant was impaired in formation of transmembrane voltage (Delta psi, inside negative) and did not grow under hypoosmotic conditions at pH 8.2 or above. This growth defect could be complemented by transformation with the plasmid encoded nqr operon. In an alkaline environment, Na+/H+ antiporters acidify the cytoplasm at the expense of the transmembrane voltage. It is proposed that, at alkaline pH and limiting Na+ concentrations, the Na+-NQR is crucial for generation of a transmembrane voltage to drive the import of H+ by electrogenic Na+/H+ antiporters. Our study provides the basis to understand the role of the Na+-NQR in pathogenicity of V. cholerae and other pathogens relying on this primary Na+ pump for respiration. (C) 2015 Elsevier B.V. All rights reserved.…
MetadatenAuthor details: | Thomas Vorburger, Ruslan NedielkovORCiDGND, Alexander Brosig, Eva Bok, Emina Schunke, Wojtek Steffen, Sonja Mayer, Friedrich Goetz, Heiko Michael MöllerORCiDGND, Julia Steuber |
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DOI: | https://doi.org/10.1016/j.bbabio.2015.12.010 |
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ISSN: | 0005-2728 |
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ISSN: | 0006-3002 |
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Pubmed ID: | https://pubmed.ncbi.nlm.nih.gov/26721205 |
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Title of parent work (English): | Biochimica et biophysica acta : Bioenergetics |
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Publisher: | Elsevier |
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Place of publishing: | Amsterdam |
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Publication type: | Article |
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Language: | English |
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Year of first publication: | 2016 |
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Publication year: | 2016 |
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Release date: | 2020/03/22 |
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Tag: | Hypoosmotic stress; Na+ homeostasis; Nuclear magnetic resonance (NMR); Respiration; Sodium transport; Vibrio cholerae |
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Volume: | 1857 |
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Number of pages: | 10 |
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First page: | 473 |
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Last Page: | 482 |
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Funding institution: | contract research of the Baden-Wurttemberg Stiftung; Forschungsprogramm [P-LS-Meth/4]; Deutsche Forschungsgemeinschaft [FR 1321/3-1, TR-SFB34] |
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Organizational units: | Mathematisch-Naturwissenschaftliche Fakultät / Institut für Chemie |
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Peer review: | Referiert |
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