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Structure and Function of the Vibrio cholerae Master Virulence Regulator ToxT
Author(s) -
Cruite Justin,
Kovacikova Gabriela,
Skorupski Karen,
Taylor Ronald,
Kull F. Jon
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.lb204
Subject(s) - vibrio cholerae , virulence , cholera toxin , pilus , biology , microbiology and biotechnology , gene , biochemistry , genetics , bacteria
The epidemic diarrheal disease cholera is caused by the ingestion of food or water contaminated with the gram‐negative bacterium Vibrio cholerae. Cholera toxin (CT) and the toxin‐coregulated pilus (TCP) are the two primary virulence factors produced by V. cholerae. The expression of both CT and TCP is activated by the AraC/XylS family transcription regulator ToxT. Previously, the crystal structure of ToxT revealed the presence of the unsaturated fatty acid (UFA), palmitoleic acid, in the ligand binding pocket. Unsaturated fatty acids, such as palmitoleic acid, are components of bile and inhibit ToxT DNA binding activity, allowing virulence to be controlled in response to the host environment. In contrast to UFAs, bicarbonate has been shown to enhance ToxT DNA binding affinity and increase virulence gene expression. In a first step towards gaining further insight into 1) how ToxT binds to DNA and activates expression, and 2) how binding to UFAs leads to conformational changes that inactivate ToxT, ToxT has been crystallized in complex with the ToxT binding region of the tcpA promoter in the presence of bicarbonate.