This Article Full Text Full Text (PDF) 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 Goerke, C. Articles by Wolz, C. Search for Related Content PubMed PubMed Citation Articles by Goerke, C. Articles by Wolz, C.

Role of Staphylococcus aureus Global Regulators sae and ^B in Virulence Gene Expression during Device-Related Infection

Institute for Medical Microbiology and Hygiene, University Hospital Tübingen, Tübingen, Germany,¹ Division of Infectious Diseases, University Hospitals Basel, Basel,² Department of Medical Microbiology, University of Zurich, Zurich, Switzerland,³ Inhibitex, Inc., Alpharetta, Georgia⁴

Received 14 September 2004/ Returned for modification 8 December 2004/ Accepted 19 January 2005

The ability of Staphylococcus aureus to adapt to different environments is due to a regulatory network comprising several loci. Here we present a detailed study of the interaction between the two global regulators sae and ^B of S. aureus and their influence on virulence gene expression in vitro, as well as during device-related infection. The expression of sae, asp23, hla, clfA, coa, and fnbA was determined in strain Newman and its isogenic saeS/R and sigB mutants by Northern analysis and LightCycler reverse transcription-PCR. There was no indication of direct cross talk between the two regulators. sae had a dominant effect on target gene expression during device-related infection. ^B seemed to be less active throughout the infection than under induced conditions in vitro.

Editor: V. J. DiRita

This article has been cited by other articles:

• Geiger, T., Goerke, C., Mainiero, M., Kraus, D., Wolz, C. (2008). The Virulence Regulator Sae of Staphylococcus aureus: Promoter Activities and Response to Phagocytosis-Related Signals. J. Bacteriol. 190: 3419-3428 [Abstract] [Full Text]  
• Li, D., Cheung, A. (2008). Repression of hla by rot Is Dependent on sae in Staphylococcus aureus. Infect. Immun. 76: 1068-1075 [Abstract] [Full Text]  
• Handke, L. D., Rogers, K. L., Olson, M. E., Somerville, G. A., Jerrells, T. J., Rupp, M. E., Dunman, P. M., Fey, P. D. (2008). Staphylococcus epidermidis saeR Is an Effector of Anaerobic Growth and a Mediator of Acute Inflammation. Infect. Immun. 76: 141-152 [Abstract] [Full Text]  
• Stapleton, M. R., Horsburgh, M. J., Hayhurst, E. J., Wright, L., Jonsson, I.-M., Tarkowski, A., Kokai-Kun, J. F., Mond, J. J., Foster, S. J. (2007). Characterization of IsaA and SceD, Two Putative Lytic Transglycosylases of Staphylococcus aureus. J. Bacteriol. 189: 7316-7325 [Abstract] [Full Text]  
• Sobke, A. C. S., Selimovic, D., Orlova, V., Hassan, M., Chavakis, T., Athanasopoulos, A. N., Schubert, U., Hussain, M., Thiel, G., Preissner, K. T., Herrmann, M. (2006). The extracellular adherence protein from Staphylococcus aureus abrogates angiogenic responses of endothelial cells by blocking Ras activation. FASEB J. 20: 2621-2623 [Abstract] [Full Text]  
• Rogasch, K., Ruhmling, V., Pane-Farre, J., Hoper, D., Weinberg, C., Fuchs, S., Schmudde, M., Broker, B. M., Wolz, C., Hecker, M., Engelmann, S. (2006). Influence of the Two-Component System SaeRS on Global Gene Expression in Two Different Staphylococcus aureus Strains.. J. Bacteriol. 188: 7742-7758 [Abstract] [Full Text]  
• Cassat, J., Dunman, P. M., Murphy, E., Projan, S. J., Beenken, K. E., Palm, K. J., Yang, S.-J., Rice, K. C., Bayles, K. W., Smeltzer, M. S. (2006). Transcriptional profiling of a Staphylococcus aureus clinical isolate and its isogenic agr and sarA mutants reveals global differences in comparison to the laboratory strain RN6390.. Microbiology 152: 3075-3090 [Abstract] [Full Text]  
• Chaturongakul, S., Boor, K. J. (2006). {sigma}B Activation under Environmental and Energy Stress Conditions in Listeria monocytogenes. Appl. Environ. Microbiol. 72: 5197-5203 [Abstract] [Full Text]  
• Liang, X., Yu, C., Sun, J., Liu, H., Landwehr, C., Holmes, D., Ji, Y. (2006). Inactivation of a Two-Component Signal Transduction System, SaeRS, Eliminates Adherence and Attenuates Virulence of Staphylococcus aureus.. Infect. Immun. 74: 4655-4665 [Abstract] [Full Text]  
• Seidl, K., Stucki, M., Ruegg, M., Goerke, C., Wolz, C., Harris, L., Berger-Bachi, B., Bischoff, M. (2006). Staphylococcus aureus CcpA Affects Virulence Determinant Production and Antibiotic Resistance.. Antimicrob. Agents Chemother. 50: 1183-1194 [Abstract] [Full Text]  
• Senn, M. M., Bischoff, M., von Eiff, C., Berger-Bachi, B. (2005). {sigma}B Activity in a Staphylococcus aureus hemB Mutant. J. Bacteriol. 187: 7397-7406 [Abstract] [Full Text]