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Infection and Immunity, September 2007, p. 4519-4527, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00491-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Inactivation of traP Has No Effect on the Agr Quorum-Sensing System or Virulence of Staphylococcus aureus{triangledown}

Lindsey N. Shaw,1 Ing-Marie Jonsson,2 Vineet K. Singh,3 Andrej Tarkowski,2 and George C. Stewart1*

Department of Veterinary Pathobiology and Bond Life Sciences Center, University of Missouri, Columbia, Missouri,1 Department of Rheumatology and Inflammation Research, University of Goteborg, Goteborg, Sweden,2 Department of Microbiology and Immunology, A.T. Still University of Health Sciences, Kirksville College of Osteopathic Medicine, Kirksville, Missouri3

Received 5 April 2007/ Returned for modification 27 April 2007/ Accepted 9 May 2007

The success of Staphylococcus aureus as a pathogen can largely be attributed to the plethora of genetic regulators encoded within its genome that temporally regulate its arsenal of virulence determinants throughout its virulence lifestyle. Arguably the most important of these is the two-component, quorum-sensing system agr. Over the last decade, the controversial presence of a second quorum-sensing system (the TRAP system) has been proposed, and it has been mooted to function as the master regulator of virulence in S. aureus by modulating agr. Mutants defective in TRAP are reported to be devoid of agr expression, lacking in hemolytic activity, essentially deficient in the secretion of virulence determinants, and avirulent in infection models. A number of research groups have questioned the validity of the TRAP findings in recent years; however, a thorough and independent analysis of its role in S. aureus physiology and pathogenesis has not been forthcoming. Therefore, we have undertaken such an analysis of the TRAP locus of S. aureus. We found that a traP mutant was equally hemolytic as the wild-type strain. Furthermore, transcriptional profiling found no alterations in the traP mutant in expression levels of agr or in expression levels of multiple agr-regulated genes (hla, sspA, and spa). Analysis of secreted and surface proteins of the traP mutant revealed no deviation in comparison to the parent. Finally, analysis conducted using a murine model of S. aureus septic arthritis revealed that, in contrast to an agr mutant, the traP mutant was just as virulent as the wild-type strain.

* Corresponding author. Mailing address: Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211. Phone: (573) 884-2866. Fax: (573) 884-9395. E-mail: stewartgc{at}missouri.edu

{triangledown} Published ahead of print on 4 June 2007.

Editor: J. B. Bliska

Infection and Immunity, September 2007, p. 4519-4527, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00491-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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