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 Lin, D.
Right arrow Articles by Slauch, J. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, D.
Right arrow Articles by Slauch, J. M.

 Previous Article  |  Next Article 

Journal of Bacteriology, January 2008, p. 87-97, Vol. 190, No. 1
0021-9193/08/$08.00+0     doi:10.1128/JB.01323-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

The Salmonella SPI1 Type Three Secretion System Responds to Periplasmic Disulfide Bond Status via the Flagellar Apparatus and the RcsCDB System{triangledown}

Dongxia Lin,1 Christopher V. Rao,2 and James M. Slauch1,3*

Department of Microbiology,1 Department of Chemical and Biomolecular Engineering,2 College of Medicine, University of Illinois, Urbana, Illinois 618013

Received 15 August 2007/ Accepted 9 October 2007

Upon contact with intestinal epithelial cells, Salmonella enterica serovar Typhimurium injects a set of effector proteins into the host cell cytoplasm via the Salmonella pathogenicity island 1 (SPI1) type III secretion system (T3SS) to induce inflammatory diarrhea and bacterial uptake. The master SPI1 regulatory gene hilA is controlled directly by three AraC-like regulators: HilD, HilC, and RtsA. Previous work suggested a role for DsbA, a periplasmic disulfide bond oxidase, in SPI1 T3SS function. RtsA directly activates dsbA, and deletion of dsbA leads to loss of SPI1-dependent secretion. We have studied the dsbA phenotypes by monitoring expression of SPI1 regulatory, structural, and effector genes. Here we present evidence that loss of DsbA independently affects SPI1 regulation and SPI1 function. The dsbA-mediated feedback inhibition of SPI1 transcription is not due to defects in the SPI1 T3SS apparatus. Rather, the transcriptional response is dependent on both the flagellar protein FliZ and the RcsCDB system, which also affects fliZ transcription. Thus, the status of disulfide bonds in the periplasm affects expression of the SPI1 system indirectly via the flagellar apparatus. RcsCDB can also affect SPI1 independently of FliZ. All regulation is through HilD, consistent with our current model for SPI1 regulation.

* 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 19 October 2007.

Journal of Bacteriology, January 2008, p. 87-97, Vol. 190, No. 1
0021-9193/08/$08.00+0     doi:10.1128/JB.01323-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Haneda, T., Winter, S. E., Butler, B. P., Wilson, R. P., Tukel, C., Winter, M. G., Godinez, I., Tsolis, R. M., Baumler, A. J. (2009). The Capsule-Encoding viaB Locus Reduces Intestinal Inflammation by a Salmonella Pathogenicity Island 1-Independent Mechanism. Infect. Immun. 77: 2932-2942 [Abstract] [Full Text]  
  • Walker, K. A., Miller, V. L. (2009). Synchronous Gene Expression of the Yersinia enterocolitica Ysa Type III Secretion System and Its Effectors. J. Bacteriol. 191: 1816-1826 [Abstract] [Full Text]  
  • Forbes, S. J., Eschmann, M., Mantis, N. J. (2008). Inhibition of Salmonella enterica Serovar Typhimurium Motility and Entry into Epithelial Cells by a Protective Antilipopolysaccharide Monoclonal Immunoglobulin A Antibody. Infect. Immun. 76: 4137-4144 [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»