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The cadA gene of Vibrio cholerae is induced during infection and plays a role in acid tolerance
Author(s) -
Merrell D. Scott,
Camilli Andrew
Publication year - 1999
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.1999.01650.x
Subject(s) - biology , vibrio cholerae , microbiology and biotechnology , pathogen , gene , rpos , lysine decarboxylase , cholera , bacteria , gene expression , biochemistry , genetics , promoter , putrescine , cadaverine , enzyme
Vibrio cholerae is a facultative pathogen of humans that must survive exposure to inorganic and organic acids in the stomach and small intestine. To learn more about the mechanisms by which this pathogen colonizes the intestinal tract, we used a recombinase gene fusion reporter to identify transcripts induced during infection in an adult rabbit model of cholera. One of the genes identified was cadA , which encodes an inducible lysine decarboxylase. CadA was also induced during infections of the suckling and adult mouse intestines, and in vitro under conditions of low pH and high lysine concentration. We show that V. cholerae is capable of mounting an acid tolerance response (ATR) to both inorganic and organic acid challenges. Mutational analyses revealed a significant role for cadA , but not for speF , which encodes an ornithine decarboxylase, in both inorganic and organic ATR. Potential roles for toxR , toxT and rpoS in ATR were examined, and it was found that toxR plays a ToxT‐independent role in mediating organic ATR, whereas rpoS played no detectable role in either ATR. Transcriptional analysis showed that the toxR defect in ATR is not caused by decreased cadA transcription. Despite induction of cadA in these animal models, competition assays revealed that neither cadA nor speF alone or together were required for colonization of suckling or adult mice. However, acid‐adapted wild‐type V. cholerae exhibited a major competitive advantage over unadapted cells during colonization of suckling mice.