Vibrio cholerae is the causative agent of cholera, a serious diarrheal disease in developing countries. V. cholerae has a unique redox driven respiration-linked sodium pump, Na⁺ translocating NADH:quinone oxidoreductase (NQR). Several reports previously showed that NQR plays an important role in virulence, metabolism, and sodium homeostasis of V. cholerae. This...
We previously found that inhibition of the TCA cycle, either through mutations or chemical inhibition, increased toxT transcription in Vibrio cholerae. In this study, we found that the addition of malonate, an inhibitor of succinate dehydrogenase (SDH), decreased toxT transcription in V. cholerae, an observation inconsistent with the previous pattern...
We previously reported that inhibition of the Na⁺ translocating NADH:ubiquinone oxidoreductase (NQR), either by chemical inhibition or mutation, increased toxT transcription in Vibrio cholerae. In this study, we revealed that the nqr mutant strain showed similar phenotypes as the Escherichia coli NADH dehydrogenase I (nuo) mutant strain (e.g. growth defect...
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SaraR. Fassio1, Yusuke Minato2, Matthew J. Quinn1, Wyatt J. Faulkner1 and
We previously reported that inhibition of the Na⁺ translocating NADH:ubiquinone oxidoreductase (NQR), either by chemical inhibition or mutation, increased toxT transcription in Vibrio cholerae. In this study, we revealed that the nqr mutant strain showed similar phenotypes as the Escherichia coli NADH dehydrogenase I (nuo) mutant strain (e.g. growth defect...
Full Text:
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Mode of action
Substrates
SaraR. Fassio1, Yusuke Minato2, Matthew J. Quinn1, Wyatt J. Faulkner1
Two virulence factors produced by Vibrio cholerae, cholera toxin (CT) and toxin-corregulated pilus (TCP), are indispensable for cholera infection. ToxT is the central regulatory protein involved in activation of CT and TCP expression. We previously reported that lack of a respiration-linked sodium-translocating NADH–ubiquinone oxidoreductase (Na⁺-NQR) significantly increases toxT transcription. In...
Two virulence factors produced by Vibrio cholerae, cholera toxin (CT) and toxin-corregulated pilus (TCP), are indispensable for cholera infection. ToxT is the central regulatory protein involved in activation of CT and TCP expression. We previously reported that lack of a respiration-linked sodium-translocating NADH–ubiquinone oxidoreductase (Na⁺-NQR) significantly increases toxT transcription. In...
Two virulence factors produced by Vibrio cholerae, cholera toxin (CT) and toxin-corregulated pilus (TCP), are indispensable for cholera infection. ToxT is the central regulatory protein involved in activation of CT and TCP expression. We previously reported that lack of a respiration-linked sodium-translocating NADH–ubiquinone oxidoreductase (Na⁺-NQR) significantly increases toxT transcription. In...
Two virulence factors produced by Vibrio cholerae, cholera toxin (CT) and toxin-corregulated pilus (TCP), are indispensable for cholera infection. ToxT is the central regulatory protein involved in activation of CT and TCP expression. We previously reported that lack of a respiration-linked sodium-translocating NADH–ubiquinone oxidoreductase (Na⁺-NQR) significantly increases toxT transcription. In...
Two virulence factors produced by Vibrio cholerae, cholera toxin (CT) and toxin-corregulated pilus (TCP), are indispensable for cholera infection. ToxT is the central regulatory protein involved in activation of CT and TCP expression. We previously reported that lack of a respiration-linked sodium-translocating NADH–ubiquinone oxidoreductase (Na⁺-NQR) significantly increases toxT transcription. In...
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., Fassio, S. R., Reddekopp, R. L., & Häse, C. C. (2014). Inhibition of the
sodium-translocating NADH
Two virulence factors produced by Vibrio cholerae, cholera toxin (CT) and toxin-corregulated pilus (TCP), are indispensable for cholera infection. ToxT is the central regulatory protein involved in activation of CT and TCP expression. We previously reported that lack of a respiration-linked sodium-translocating NADH–ubiquinone oxidoreductase (Na⁺-NQR) significantly increases toxT transcription. In...