This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Golubeva, Y. A.
Right arrow Articles by Slauch, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Golubeva, Y. A.
Right arrow Articles by Slauch, J. M.

 Previous Article  |  Next Article 

Journal of Bacteriology, November 2006, p. 7853-7861, Vol. 188, No. 22
0021-9193/06/$08.00+0     doi:10.1128/JB.00706-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Salmonella enterica Serovar Typhimurium Periplasmic Superoxide Dismutase SodCI Is a Member of the PhoPQ Regulon and Is Induced in Macrophages{triangledown}

Yekaterina A. Golubeva1 and James M. Slauch1,2*

Department of Microbiology,1 College of Medicine, University of Illinois, Urbana, Illinois 618012

Received 17 May 2006/ Accepted 29 August 2006

Salmonella enterica serovar Typhimurium replicates within host macrophages during the systemic stage of infection. In the macrophage, the bacteria must survive the respiratory burst that produces superoxide. Serovar Typhimurium strain 14028 produces two periplasmic superoxide dismutases, SodCI and SodCII, but only SodCI contributes to virulence. Although we have shown that this is primarily due to differences in the two proteins, evidence suggests differential regulation of the two genes. Using transcriptional sodCI- and sodCII-lac fusions, we show that sodCII is under the control of the RpoS sigma factor, as was known for the Escherichia coli ortholog, sodC. In contrast, we show that sodCI is transcriptionally controlled by the PhoPQ two-component regulatory system, which regulates an array of virulence genes required for macrophage survival. Introduction of a phoP-null mutation into the sodCI fusion strain resulted in a decrease in transcription and loss of regulation. The sodCI-lac fusion showed high-level expression in a background containing a phoQ constitutive allele. The sodCI gene is induced 15-fold in bacteria recovered from either the tissue culture macrophages or the spleens of infected mice. Induction in macrophages is dependent on PhoP. The sodCII fusion was induced three- to fourfold in macrophages and animals; this induction was unaffected by loss of PhoP. Thus, sodCI, which is horizontally transferred by the Gifsy-2 phage, is regulated by PhoPQ such that it is induced at the appropriate time and place to combat phagocytic superoxide.

* Corresponding author. Mailing address: Department of Microbiology, University of Illinois, B103 Chemical and Life Sciences Laboratory, 601 S. Goodwin Ave., Urbana, IL 61801. Phone: (217) 244-1956. Fax: (217) 244-6697. E-mail: slauch{at}uiuc.edu.

{triangledown} Published ahead of print on 15 September 2006.

Journal of Bacteriology, November 2006, p. 7853-7861, Vol. 188, No. 22
0021-9193/06/$08.00+0     doi:10.1128/JB.00706-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ammendola, S., Pasquali, P., Pacello, F., Rotilio, G., Castor, M., Libby, S. J., Figueroa-Bossi, N., Bossi, L., Fang, F. C., Battistoni, A. (2008). Regulatory and Structural Differences in the Cu,Zn-Superoxide Dismutases of Salmonella enterica and Their Significance for Virulence. J. Biol. Chem. 283: 13688-13699 [Abstract] [Full Text]  
  • Krishnakumar, R., Kim, B., Mollo, E. A., Imlay, J. A., Slauch, J. M. (2007). Structural Properties of Periplasmic SodCI That Correlate with Virulence in Salmonella enterica Serovar Typhimurium. J. Bacteriol. 189: 4343-4352 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»