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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Adhikari, R. P.
Right arrow Articles by Novick, R. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Adhikari, R. P.
Right arrow Articles by Novick, R. P.

 Previous Article  |  Next Article 

Infection and Immunity, September 2007, p. 4534-4540, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00679-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

A Nonsense Mutation in agrA Accounts for the Defect in agr Expression and the Avirulence of Staphylococcus aureus 8325-4 traP::kan{triangledown}

Rajan P. Adhikari,1 Staffan Arvidson,2 and Richard P. Novick1*

Program in Molecular Pathogenesis, Kimmel Center for Biology and Medicine, Skirball Institute of Biomolecular Medicine, and Departments of Microbiology and Medicine, New York University Medical Center, New York, New York 10016,1 Department of Microbiology Tumor and Cell Biology, Karolinska Institute, S 171 77 Stockholm, Sweden2

Received 16 May 2007/ Returned for modification 14 June 2007/ Accepted 20 June 2007

TraP is a triply phosphorylated staphylococcal protein that has been hypothesized to be the mediator of a second Staphylococcus aureus quorum-sensing system, "SQS1," that controls expression of the agr system and therefore is essential for the organism's virulence. This hypothesis was based on the loss of agr expression and virulence by a traP mutant of strain 8325-4 and was supported by full complementation of both phenotypic defects by the cloned traP gene in strain NB8 (Y. Gov, I. Borovok, M. Korem, V. K. Singh, R. K. Jayaswal, B. J. Wilkinson, S. M. Rich, and N. Balaban, J. Biol. Chem. 279:14665-14672, 2004), in which the wild-type traP gene was expressed in trans in the 8325-4 traP mutant. We initiated a study of the mechanism by which TraP activates agr and found that the traP mutant strain used for this and other recently published studies has a second mutation, an adventitious stop codon in the middle of agrA, the agr response regulator. The traP mutation, once separated from the agrA defect by outcrossing, had no effect on agr expression or virulence, indicating that the agrA defect accounts fully for the lack of agr expression and for the loss of virulence attributed to the traP mutation. In addition, DNA sequencing showed that the agrA gene in strain NB8 (Gov et al., J. Biol. Chem., 2004), in contrast to that in the agr-defective 8325-4 traP mutant strain, had the wild-type sequence; further, the traP mutation in that strain, when outcrossed, also had no effect on agr expression.

* Corresponding author. Mailing address: Program in Molecular Pathogenesis, Skirball Institute, and Departments of Microbiology and Medicine, New York University Medical Center, New York, NY 10016. Phone: (212) 263-6290. Fax: (212) 263-5711. E-mail: novick{at}saturn.med.nyu.edu

{triangledown} Published ahead of print on 2 July 2007.

Editor: J. B. Bliska

Infection and Immunity, September 2007, p. 4534-4540, Vol. 75, No. 9
0019-9567/07/$08.00+0     doi:10.1128/IAI.00679-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Wirtz, C., Witte, W., Wolz, C., Goerke, C. (2009). Transcription of the phage-encoded Panton-Valentine leukocidin of Staphylococcus aureus is dependent on the phage life-cycle and on the host background. Microbiology 155: 3491-3499 [Abstract] [Full Text]  
  • Coelho, L. R., Souza, R. R., Ferreira, F. A., Guimaraes, M. A., Ferreira-Carvalho, B. T., Figueiredo, A. M. S. (2008). agr RNAIII divergently regulates glucose-induced biofilm formation in clinical isolates of Staphylococcus aureus. Microbiology 154: 3480-3490 [Abstract] [Full Text]  
  • 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]  
  • Kiran, M. D., Adikesavan, N. V., Cirioni, O., Giacometti, A., Silvestri, C., Scalise, G., Ghiselli, R., Saba, V., Orlando, F., Shoham, M., Balaban, N. (2008). Discovery of a Quorum-Sensing Inhibitor of Drug-Resistant Staphylococcal Infections by Structure-Based Virtual Screening. Mol. Pharmacol. 73: 1578-1586 [Abstract] [Full Text]  
  • Meredith, T. C., Swoboda, J. G., Walker, S. (2008). Late-Stage Polyribitol Phosphate Wall Teichoic Acid Biosynthesis in Staphylococcus aureus. J. Bacteriol. 190: 3046-3056 [Abstract] [Full Text]  


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