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Journal of Bacteriology, January 2007, p. 351-362, Vol. 189, No. 2
0021-9193/07/$08.00+0     doi:10.1128/JB.01297-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Global Gene Expression and Phenotypic Analysis of a Vibrio cholerae rpoH Deletion Mutant{triangledown}

Leyla Slamti, Jonathan Livny, and Matthew K. Waldor*

Department of Molecular Biology and Microbiology, Tufts University School of Medicine, and Howard Hughes Medical Institute, 136 Harrison Avenue, Boston, Massachusetts 02111

Received 16 August 2006/ Accepted 26 October 2006

Vibrio cholerae, the cause of cholera, can grow in a variety of environments outside of human hosts. During infection, this pathogen must adapt to significant environmental alterations, including the elevated temperature of the human gastrointestinal tract. {sigma}32, an alternative sigma factor encoded by rpoH, activates transcription of genes involved in the heat shock response in several bacterial species. Here, we assessed the role of {sigma}32 in V. cholerae physiology. In aggregate, our findings suggest that {sigma}32 promotes V. cholerae growth at temperatures ranging at least from 15°C to 42°C. Growth of the rpoH mutant was severely attenuated within the suckling mouse intestine, suggesting that {sigma}32-regulated genes are critical for V. cholerae adaptation to conditions within the gastrointestinal tract. We defined the V. cholerae RpoH regulon by comparing the whole-genome transcription profiles of the wild-type and rpoH mutant strains after a temperature up-shift. Most of the V. cholerae genes expressed in an RpoH-dependent manner after heat shock encode proteins that influence protein fate, such as proteases and chaperones, or are of unknown function. Bioinformatic analyses of the microarray data were used to define a putative {sigma}32 consensus binding sequence and subsequently to identify genes that are likely to be directly regulated by RpoH in the whole V. cholerae genome.

* Corresponding author. Mailing address: Department of Molecular Biology and Microbiology, Tufts University School of Medicine, and Howard Hughes Medical Institute, 136 Harrison Avenue, Boston, MA 02111. Phone: (617) 636-2730. Fax: (617) 636-2723. E-mail: matthew.waldor{at}tufts.edu.

{triangledown} Published ahead of print on 3 November 2006.

Journal of Bacteriology, January 2007, p. 351-362, Vol. 189, No. 2
0021-9193/07/$08.00+0     doi:10.1128/JB.01297-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Grall, N., Livny, J., Waldor, M., Barel, M., Charbit, A., Meibom, K. L. (2009). Pivotal role of the Francisella tularensis heat-shock sigma factor RpoH. Microbiology 155: 2560-2572 [Abstract] [Full Text]  


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