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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.


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