JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
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 McNamara, P. J.
Right arrow Articles by Iandolo, J. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McNamara, P. J.
Right arrow Articles by Iandolo, J. J.

J Bacteriol, May 1998, p. 2609-2615, Vol. 180, No. 10
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Genetic Instability of the Global Regulator agr Explains the Phenotype of the xpr Mutation in Staphylococcus aureus KSI9051

Peter J. McNamara and John J. Iandolo*

Department of Microbiology and Immunology, University of Oklahoma Health Science Center, Oklahoma City, Oklahoma 73190

Received 16 October 1997/Accepted 17 March 1998

Staphylococcus aureus KSI9051 has a complex mutation that was associated with the aberrant expression of cell surface and extracellular proteins (M. S. Smeltzer, M. E. Hart, and J. J. Iandolo, J. Bacteriol. 61:919-925, 1993). This mutation was named xpr, although no specific gene was identified. Here this mutation is referred to as Delta 1058::Tn551. In this study, we show that in strain KSI9051, the Delta 1058::Tn551 mutation occurred coincidentally with a frameshift in agrC that is expected to truncate the sensor component of the known staphylococcal global regulatory locus agr. Remarkably, pleiotropic mutations affecting cell surface and extracellular proteins are generated at frequencies approaching 50% upon the transduction of erythromycin resistance (Emr) encoded by Delta 1058::Tn551 from S. aureus KSI905 back to its parental strain, S6C. Three independent isolates created in the manner of KSI9051 contained mutations within agrC. Each isolate had different mutations, suggesting that the transduction of Emr encoded by Delta 1058::Tn551 affects the stability of agrC in S6C. In similar experiments with strains from an S. aureus 8325 genetic background, a mutant AgrC phenotype could not be isolated, implying that strain S6 has aberrant genetic behavior. A comparison of the nucleotide sequences of AgrC from several strains revealed seven errors in the GenBank entry for agr (X52543); these data were confirmed with plasmid pRN6650, the original wild-type clone of agr.


* Corresponding author. Mailing address: Department of Microbiology & Immunology, University of Oklahoma Health Science Center, P.O. Box 26901, Oklahoma City, OK 73190. Phone: (405) 271-2133. Fax: (405) 271-3117. E-mail: John-Iandolo{at}ouhsc.edu.


J Bacteriol, May 1998, p. 2609-2615, Vol. 180, No. 10
0021-9193/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 1998 by the American Society for Microbiology. All rights reserved.