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Infection and Immunity, April 2009, p. 1383-1388, Vol. 77, No. 4
0019-9567/09/$08.00+0 doi:10.1128/IAI.01156-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

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Xiao Xu,2,
Biao Kan,2
Rahul V. Kulkarni,3 and
Jun Zhu1,4*
Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania 19104,1 The State Key Laboratory for Infectious Disease Prevention and Control, National Institute for Communicable Disease Control and Prevention, Beijing, China,2 Department of Physics, Virginia Polytechnic Institute and State University, Blacksburg, Virginia 24061,3 The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, China4
Received 16 September 2008/ Returned for modification 21 October 2008/ Accepted 12 January 2009
The pathogen Vibrio cholerae uses a large number of coordinated transcriptional regulatory events to transition from its environmental reservoir to the host and establish itself at its preferred colonization site at the host intestinal mucosa. The key regulator in this process is the AraC/XylS family transcription factor, ToxT, which plays critical roles in pathogenesis, including the regulation of two type IV pili, the anticolonization factor mannose-sensitive hemagglutinin and the toxin-coregulated pilus. Previously, it was thought ToxT required dimerization in order to effect transcriptional regulation at its cognate promoters. Here, we present evidence that ToxT directly represses transcription of the msh operon by binding to three promoters within this operon and that dimerization may not be required for transcriptional repression of target promoters by ToxT, suggesting that this regulator uses different mechanisms to modulate the transcriptional repertoire of V. cholerae.
Published ahead of print on 21 January 2009.
A.H. and X.X. contributed equally to this study.
Present address: Center for Genome Sciences, Washington University, St. Louis, MO 63108.
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