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Coordinate expression of many virulence genes in the human pathogenVibrio cholerae is controlled by the ToxR, TcpP, and ToxT proteins. These proteins function in a regulatory cascade in which ToxR and TcpP, two inner membrane proteins, are required to activatetoxT and ToxT is the direct activator of virulence gene expression. ToxT-activated genes include those whose products are required for the biogenesis of cholera toxin (CTX) and the toxin-coregulated pilus, the major subunit of which is TcpA. This work examined control oftoxT transcription. We tested a model whereby activation oftoxT by ToxR and TcpP is required to prime an autoregulatory loop in which ToxT-dependent transcription of thetcpA promoter reads through a proposed terminator between thetcpF andtoxT genes to result in continued ToxT production. Primer extension analysis of RNA from wild-type classical strain O395 showed that there are two products encodingtoxT , one of which is longer than the other by 105 bp. Deletion of thetoxT promoter (toxTΔpro ) resulted in the abolishment oftoxT transcription, as predicted. Deletion of thetcpA promoter (tcpAΔpro ) had no effect on subsequent detection of the smallertoxT primer extension product, but the largertoxT product was not detected, indicating that this product may be the result of transcription from thetcpA promoter and not of initiation directly upstream oftoxT . Neither mutant strain produced detectable TcpA, but the CTX levels of the strains were different. ThetoxTΔpro strain produced little detectable CTX, while thetcpAΔpro strain produced CTX levels intermediate between those of the wild-type andtoxTΔpro strains. Dependence oftoxT transcription on TcpP and TcpH was confirmed by analyzing RNAs from strains carrying deletions in the genes encoding these regulators. ThetcpP defect resulted in undetectabletoxT transcription, whereas thetcpH mutation led to a diminishing oftoxT RNA but not complete abolishment. Taken together, these results suggest thattoxT transcription is dependent on two different promoters; one is directly upstream and is activated in part by TcpP and TcpH, and the other is much further upstream and is activated by ToxT.

Analysis of an Autoregulatory Loop Controlling ToxT, Cholera Toxin, and Toxin-Coregulated Pilus Production in Vibrio cholerae