Inactivation of traP has no effect on the agr quorum-sensing system or virulence of Staphylococcus aureus.
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.
Shaw
Lindsey N
LN
Department of Veterinary Pathobiology, University of Missouri, Columbia, MO 65211, USA.
Jonsson
Ing-Marie
IM
Singh
Vineet K
VK
Tarkowski
Andrej
A
Stewart
George C
GC
D000818:Animals; D001170:Arthritis, Infectious / Q000235:genetics / Q000378:metabolism / Q000382:microbiology; D001426:Bacterial Proteins / Q000235:genetics* / Q000502:physiology*; D004195:Disease Models, Animal; D005260:Female; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology*; D020868:Gene Silencing; D006461:Hemolysis / Q000235:genetics; D051379:Mice; D053038:Quorum Sensing / Q000235:genetics / Q000502:physiology*; D016601:RNA-Binding Proteins / Q000235:genetics*; D013203:Staphylococcal Infections / Q000235:genetics / Q000378:metabolism / Q000382:microbiology; D013211:Staphylococcus aureus / Q000235:genetics / Q000472:pathogenicity*; D015534:Trans-Activators / Q000235:genetics / Q000502:physiology*; D014157:Transcription Factors / Q000172:deficiency* / Q000235:genetics*; D014774:Virulence
C095698:Agr protein, Staphylococcus aureus; D001426:Bacterial Proteins; C079092:MtrB protein, Bacteria; D016601:RNA-Binding Proteins; D015534:Trans-Activators; D014157:Transcription Factors