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
Google Scholar
Right arrow Articles by Epler, C. R.
Right arrow Articles by Picking, W. D.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Epler, C. R.
Right arrow Articles by Picking, W. D.

 Previous Article  |  Next Article 

Infection and Immunity, July 2009, p. 2754-2761, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00190-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Liposomes Recruit IpaC to the Shigella flexneri Type III Secretion Apparatus Needle as a Final Step in Secretion Induction {triangledown}

Chelsea R. Epler,1 Nicholas E. Dickenson,2 Andrew J. Olive,1,{dagger} Wendy L. Picking,2 and William D. Picking1,2*

Department of Molecular Biosciences,1 Higuchi Bioscience Center, University of Kansas, Lawrence, Kansas 660452

Received 18 February 2009/ Returned for modification 23 March 2009/ Accepted 29 April 2009

Shigella flexneri contact with enterocytes induces a burst of protein secretion via its type III secretion apparatus (TTSA) as an initial step in cellular invasion. We have previously reported that IpaD is positioned at the TTSA needle tip (M. Espina et al., Infect. Immuno. 74:4391-4400, 2006). From this position, IpaD senses small molecules in the environment to control the presentation of IpaB to the needle tip. This step occurs without type III secretion induction or IpaC recruitment to the S. flexneri surface. IpaC is then transported to the S. flexneri surface when target cell lipids are added, and this event presumably mimics host cell contact. Unlike IpaB mobilization, IpaC surface presentation is closely linked to secretion induction. This study demonstrates that sphingomyelin and cholesterol are key players in type III secretion induction and that they appear to interact with IpaB to elicit IpaC presentation at the TTSA needle tip. Furthermore, IpaB localization at the needle tip prior to membrane contact provides the optimal set of conditions for host cell invasion. Thus, the S. flexneri type III secretion system can be induced in a stepwise manner, with the first step being the stable association of IpaD with the needle tip, the second step being the sensing of small molecules by IpaD to mobilize IpaB to the tip, and the third step being the interaction of lipids with IpaB to induce IpaC localization at the needle tip concomitant with translocon insertion into the host membrane and type III secretion induction.

* Corresponding author. Mailing address: Department of Molecular Biosciences, University of Kansas, 1200 Sunnyside Avenue, Lawrence, KS 66045. Phone: (785) 864-3299. Fax: (785) 864-5294. E-mail: picking{at}ku.edu

{triangledown} Published ahead of print on 11 May 2009.

Editor: A. J. Bäumler

{dagger} Present address: Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.

Infection and Immunity, July 2009, p. 2754-2761, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00190-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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