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

 Previous Article  |  Next Article 

Journal of Bacteriology, April 2008, p. 2726-2738, Vol. 190, No. 8
0021-9193/08/$08.00+0     doi:10.1128/JB.01553-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

ExoS Controls the Cell Contact-Mediated Switch to Effector Secretion in Pseudomonas aeruginosa ^,

Michelle Cisz, Pei-Chung Lee, and Arne Rietsch^*

Department of Molecular Biology and Microbiology, Case Western Reserve University, 10900 Euclid Ave., Cleveland, Ohio 44106-4960

Received 26 September 2007/ Accepted 3 November 2007

Type III secretion is used by many gram-negative bacterial pathogens to directly deliver protein toxins (effectors) into targeted host cells. In all cases, secretion of effectors is triggered by host cell contact, although the mechanism is unclear. In Pseudomonas aeruginosa, expression of all type III secretion-related genes is up-regulated when secretion is triggered. We were able to visualize this process using a green fluorescent protein reporter system and to use it to monitor the ability of bacteria to trigger effector secretion on cell contact. Surprisingly, the action of one of the major type III secreted effectors, ExoS, prevented triggering of type III secretion by bacteria that subsequently attached to cells, suggesting that triggering of secretion is feedback regulated. Evidence is presented that translocation (secretion of effectors across the host cell plasma membrane) of ExoS is indeed self-regulated and that this inhibition of translocation can be achieved by either of its two enzymatic activities. The translocator proteins PopB, PopD, and PcrV are secreted via the type III secretion system and are required for pore formation and translocation of effectors across the host cell plasma membrane. Here we present data that secretion of translocators is in fact not controlled by calcium, implying that triggering of effector secretion on cell contact represents a switch in secretion specificity, rather than a triggering of secretion per se. The requirement for a host cell cofactor to control effector secretion may help explain the recently observed phenomenon of target cell specificity in both the Yersinia and P. aeruginosa type III secretion systems.

---

* Corresponding author. Mailing address: Department of Molecular Biology and Microbiology, Case Western Reserve University School of Medicine, 10900 Euclid Ave., Cleveland, OH 44106-4960. Phone: (216) 368-2249. Fax: (216) 368-3055. E-mail: arne.rietsch{at}case.edu

Published ahead of print on 26 November 2007.

Supplemental material for this article may be found at http://jb.asm.org/.

---

Journal of Bacteriology, April 2008, p. 2726-2738, Vol. 190, No. 8
0021-9193/08/$08.00+0     doi:10.1128/JB.01553-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Isaksson, E. L., Aili, M., Fahlgren, A., Carlsson, S. E., Rosqvist, R., Wolf-Watz, H. (2009). The Membrane Localization Domain Is Required for Intracellular Localization and Autoregulation of YopE in Yersinia pseudotuberculosis. Infect. Immun. 77: 4740-4749 [Abstract] [Full Text]  
• Urbanowski, M. L., Yahr, T. L. (2008). Limiting Too Much of a Good Thing: a Negative Feedback Mechanism Prevents Unregulated Translocation of Type III Effector Proteins. J. Bacteriol. 190: 2643-2644 [Full Text]