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...
We found that a strains of Yersinia pestis (KIM5) which lacked the nhaA gene was fully attenuated in a plague model. This gene produces a protein of the sodium-proton antiporter family which expel sodium ions from the bacterial cytoplasm in exchange for hydrogen ions, or protons, from the surrounding environment....
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...
The pathogen Vibrio cholerae uses cations as a primary currency of virulence
and environmental persistence, using gradients of those cations to move, acquire
nutrients, and control virulence gene expression. An understanding of the overlapping
roles of bioenergetics and chemotaxis in the virulence and environmental survival of
V. cholerae issues from...