Previous Article | Next Article 
Infection and Immunity, February 2001, p. 737-743, Vol. 69, No. 2
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.2.737-743.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Salmonella Pathogenicity Island 2-Encoded Proteins
SseC and SseD Are Essential for Virulence and Are Substrates of the
Type III Secretion System
Joanna R.
Klein and
Bradley D.
Jones*
Department of Microbiology, University of
Iowa School of Medicine, Iowa City, Iowa 52242-1109
Received 28 August 2000/Returned for modification 18 October
2000/Accepted 8 November 2000
Survival of Salmonella enterica serovar Typhimurium
within host phagocytic cells is a critical step in establishing
systemic infection in mice. Genes within Salmonella
pathogenicity island 2 (SPI-2) encode a type III secretion system that
is required for establishment of systemic infection. Several proteins
encoded by SPI-2 have homology to type III secreted proteins from
enteropathogenic Escherichia coli and Yersinia
and, based on that homology, are predicted to be secreted through the
SPI-2 type III secretion system. We have investigated the roles of two
of these proteins, SseC and SseD. We demonstrate here that the SseD
protein is required for systemic Salmonella infection of
the mouse, and we confirmed the virulence requirement for the SseC
protein. Experiments were performed, using cellular fractionation and
immunoblotting, to identify the subcellular location of the SseC and
SseD proteins. Both proteins were found to localize predominantly to
the bacterial cell membrane. In addition, our work revealed that SseC
and SseD are exposed to the extracellular environment and are loosely
associated with the bacterial membrane. Furthermore, localization of
SseC and SseD to the bacterial membrane was found to require a
functional SPI-2 type III secretion system. Collectively, these results
indicate that the SseC and SseD proteins are secreted by the SPI-2 type III secretion system to the bacterial membrane in order to perform their virulence functions.
*
Corresponding author. Mailing address: Department of
Microbiology, University of Iowa College of Medicine, 3-330 Bowen
Science Bldg., Iowa City, IA 52242. Phone: (319) 353-5457. Fax: (319) 335-9006. E-mail:bjones{at}blue.weeg.uiowa.edu.
Infection and Immunity, February 2001, p. 737-743, Vol. 69, No. 2
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.2.737-743.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
This article has been cited by other articles:
-
Miki, T., Shibagaki, Y., Danbara, H., Okada, N.
(2009). Functional Characterization of SsaE, a Novel Chaperone Protein of the Type III Secretion System Encoded by Salmonella Pathogenicity Island 2. J. Bacteriol.
191: 6843-6854
[Abstract]
[Full Text]
-
Kim, H. G., Kim, B. H., Kim, J. S., Eom, J. S., Bang, I.-S., Bang, S. H., Lee, I. S., Park, Y. K.
(2008). N-terminal residues of SipB are required for its surface localization on Salmonella enterica serovar Typhimurium. Microbiology
154: 207-216
[Abstract]
[Full Text]
-
Wapling, J., Moore, K. L., Sonza, S., Mak, J., Tachedjian, G.
(2005). Mutations That Abrogate Human Immunodeficiency Virus Type 1 Reverse Transcriptase Dimerization Affect Maturation of the Reverse Transcriptase Heterodimer. J. Virol.
79: 10247-10257
[Abstract]
[Full Text]
-
Hapfelmeier, S., Stecher, B., Barthel, M., Kremer, M., Muller, A. J., Heikenwalder, M., Stallmach, T., Hensel, M., Pfeffer, K., Akira, S., Hardt, W.-D.
(2005). The Salmonella Pathogenicity Island (SPI)-2 and SPI-1 Type III Secretion Systems Allow Salmonella Serovar typhimurium to Trigger Colitis via MyD88-Dependent and MyD88-Independent Mechanisms. J. Immunol.
174: 1675-1685
[Abstract]
[Full Text]
-
Zurawski, D. V., Stein, M. A.
(2004). The SPI2-encoded SseA chaperone has discrete domains required for SseB stabilization and export, and binds within the C-terminus of SseB and SseD. Microbiology
150: 2055-2068
[Abstract]
[Full Text]
-
Hansen-Wester, I., Chakravortty, D., Hensel, M.
(2004). Functional Transfer of Salmonella Pathogenicity Island 2 to Salmonella bongori and Escherichia coli. Infect. Immun.
72: 2879-2888
[Abstract]
[Full Text]
-
Boddicker, J. D., Jones, B. D.
(2004). Lon Protease Activity Causes Down-Regulation of Salmonella Pathogenicity Island 1 Invasion Gene Expression after Infection of Epithelial Cells. Infect. Immun.
72: 2002-2013
[Abstract]
[Full Text]
-
Ruiz-Albert, J., Mundy, R., Yu, X.-J., Beuzon, C. R., Holden, D. W.
(2003). SseA is a chaperone for the SseB and SseD translocon components of the Salmonella pathogenicity-island-2-encoded type III secretion system. Microbiology
149: 1103-1111
[Abstract]
[Full Text]
-
Freeman, J. A., Rappl, C., Kuhle, V., Hensel, M., Miller, S. I.
(2002). SpiC Is Required for Translocation of Salmonella Pathogenicity Island 2 Effectors and Secretion of Translocon Proteins SseB and SseC. J. Bacteriol.
184: 4971-4980
[Abstract]
[Full Text]
-
Hindle, Z., Chatfield, S. N., Phillimore, J., Bentley, M., Johnson, J., Cosgrove, C. A., Ghaem-Maghami, M., Sexton, A., Khan, M., Brennan, F. R., Everest, P., Wu, T., Pickard, D., Holden, D. W., Dougan, G., Griffin, G. E., House, D., Santangelo, J. D., Khan, S. A., Shea, J. E., Feldman, R. G., Lewis, D. J. M.
(2002). Characterization of Salmonella enterica Derivatives Harboring Defined aroC and Salmonella Pathogenicity Island 2 Type III Secretion System (ssaV) Mutations by Immunization of Healthy Volunteers. Infect. Immun.
70: 3457-3467
[Abstract]
[Full Text]
-
Hansen-Wester, I., Stecher, B., Hensel, M.
(2002). Type III Secretion of Salmonella enterica Serovar Typhimurium Translocated Effectors and SseFG. Infect. Immun.
70: 1403-1409
[Abstract]
[Full Text]
-
Nikolaus, T., Deiwick, J., Rappl, C., Freeman, J. A., Schroder, W., Miller, S. I., Hensel, M.
(2001). SseBCD Proteins Are Secreted by the Type III Secretion System of Salmonella Pathogenicity Island 2 and Function as a Translocon. J. Bacteriol.
183: 6036-6045
[Abstract]
[Full Text]
-
Jones, M. A., Wigley, P., Page, K. L., Hulme, S. D., Barrow, P. A.
(2001). Salmonella enterica Serovar Gallinarum Requires the Salmonella Pathogenicity Island 2 Type III Secretion System but Not the Salmonella Pathogenicity Island 1 Type III Secretion System for Virulence in Chickens. Infect. Immun.
69: 5471-5476
[Abstract]
[Full Text]
-
Gallois, A., Klein, J. R., Allen, L.-A. H., Jones, B. D., Nauseef, W. M.
(2001). Salmonella Pathogenicity Island 2-Encoded Type III Secretion System Mediates Exclusion of NADPH Oxidase Assembly from the Phagosomal Membrane. J. Immunol.
166: 5741-5748
[Abstract]
[Full Text]