AAC
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 Bischoff, M.
Right arrow Articles by Berger-Bächi, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bischoff, M.
Right arrow Articles by Berger-Bächi, B.

 Previous Article  |  Next Article 

Antimicrobial Agents and Chemotherapy, June 2001, p. 1714-1720, Vol. 45, No. 6
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.6.1714-1720.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Teicoplanin Stress-Selected Mutations Increasing sigma B Activity in Staphylococcus aureus

Markus Bischoff* and Brigitte Berger-Bächi

Institute of Medical Microbiology, University of Zürich, CH8028 Zürich, Switzerland

Received 1 December 2000/Returned for modification 29 January 2001/Accepted 12 March 2001

A natural rsbU mutant of Staphylococcus aureus, unable to activate the alternative transcription factor sigma B via the RsbU pathway and therefore forming unpigmented colonies, produced first-step teicoplanin-resistant mutants upon selection for growth in the presence of teicoplanin, of which the majority were of an intense orange color. By using an asp23 promoter-luciferase fusion as an indicator, the pigmented mutants were shown to express increased sigma B activity. Increased sigma B activity was associated with point mutations in rsbW, releasing sigma B from sequestration by the anti-sigma factor RsbW, or to promoter mutations increasing the sigma B/RsbW ratio. Genetic manipulations involving the sigB operon suggested that the mutations within the operon were associated with the increase in teicoplanin resistance. The upregulation of sigma B suggests that a sigma B-controlled gene(s) is directly or indirectly involved in the development of teicoplanin resistance in S. aureus. Carotenoids do not contribute to teicoplanin resistance, since inactivation of the dehydrosqualene synthase gene crtM abolished pigment formation without affecting teicoplanin resistance. The relevant sigma B-controlled target genes involved in teicoplanin resistance remain to be identified.

* Corresponding author. Mailing address: Institute of Medical Microbiology, University of Zürich, Gloriastr. 32, CH8028 Zürich, Switzerland. Phone: 41 1 634 26 70. Fax: 41 1 634 49 06. E-mail: bischoff{at}immv.unizh.ch.

Antimicrobial Agents and Chemotherapy, June 2001, p. 1714-1720, Vol. 45, No. 6
0066-4804/01/$04.00+0   DOI: 10.1128/AAC.45.6.1714-1720.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:



Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Clin. Vaccine Immunol. Clin. Microbiol. Rev.
J. Clin. Microbiol. ALL ASM JOURNALS

Copyright © 2001 by the American Society for Microbiology. All rights reserved.