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Infection and Immunity, April 2008, p. 1617-1627, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01337-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Role of Cyclic Di-GMP during El Tor Biotype Vibrio cholerae Infection: Characterization of the In Vivo-Induced Cyclic Di-GMP Phosphodiesterase CdpA{triangledown}

Rita Tamayo, Stefan Schild, Jason T. Pratt, and Andrew Camilli*

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

Received 4 October 2007/ Returned for modification 1 December 2007/ Accepted 17 January 2008

In Vibrio cholerae, the second messenger cyclic di-GMP (c-di-GMP) positively regulates biofilm formation and negatively regulates virulence and is proposed to play an important role in the transition from persistence in the environment to survival in the host. Herein we describe a characterization of the infection-induced gene cdpA, which encodes both GGDEF and EAL domains, which are known to mediate diguanylate cyclase and c-di-GMP phosphodiesterase (PDE) activities, respectively. CdpA is shown to possess PDE activity, and this activity is regulated by its inactive degenerate GGDEF domain. CdpA inhibits biofilm formation but has no effect on colonization of the infant mouse small intestine. Consistent with these observations, cdpA is expressed during in vitro growth in a biofilm but is not expressed in vivo until the late stage of infection, after colonization has occurred. To test for a role of c-di-GMP in the early stages of infection, we artificially increased c-di-GMP and observed reduced colonization. This was attributed to a significant reduction in toxT transcription during infection. Cumulatively, these results support a model of the V. cholerae life cycle in which c-di-GMP must be down-regulated early after entering the small intestine and maintained at a low level to allow virulence gene expression, colonization, and motility at appropriate stages of infection.

* Corresponding author. Mailing address: Howard Hughes Medical Institute and the Department of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, MA 02111. Phone: (617) 636-2144. Fax: (617) 636-2175. E-mail: andrew.camilli{at}tufts.edu

{triangledown} Published ahead of print on 28 January 2008.

Editor: A. J. Bäumler

Infection and Immunity, April 2008, p. 1617-1627, Vol. 76, No. 4
0019-9567/08/$08.00+0     doi:10.1128/IAI.01337-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Pratt, J. T., McDonough, E., Camilli, A. (2009). PhoB Regulates Motility, Biofilms, and Cyclic di-GMP in Vibrio cholerae. J. Bacteriol. 191: 6632-6642 [Abstract] [Full Text]  
  • Minasov, G., Padavattan, S., Shuvalova, L., Brunzelle, J. S., Miller, D. J., Basle, A., Massa, C., Collart, F. R., Schirmer, T., Anderson, W. F. (2009). Crystal Structures of YkuI and Its Complex with Second Messenger Cyclic Di-GMP Suggest Catalytic Mechanism of Phosphodiester Bond Cleavage by EAL Domains. J. Biol. Chem. 284: 13174-13184 [Abstract] [Full Text]  
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