The purpose of this project is to study which methyl-accepting chemotaxis proteins (MCPs) are related to chemotaxis of Vibrio cholerae. 44 MCP mutant strains were tested in seven different chemoattractants and the resulting swarm circle size was compared to that of C6706 lac-Z wildtype. Several genes were identified that resulted...
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 a gram-negative gammaproteobacteria, well
known for causing the watery-diarrheal disease Cholera. V. cholerae is
endemic to the marine and freshwater ecosystems of India and
surrounding aquatic environments within that region. Primary
reservoirs include brackish water and estuaries. The primary symptom
is rapid dehydration due to watery diarrhea....
Vibrio tubiashii has been linked to disease outbreaks in molluscan species, including oysters, geoducks, and clams. In particular, oyster hatcheries in the Pacific Northwest have been plagued by intermittent vibriosis since 2006. Accurate detection of vibrios, including V. tubiashii, is critical to the hatcheries in order to allow for rapid...
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...
Full Text:
., Fassio, S. R., Reddekopp, R. L., & Häse, C. C. (2014). Inhibition of the
sodium-translocating NADH
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...
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...