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Teicoplanin stress-selected mutations increasing sigma(B) activity in Staphylococcus aureus


Bischoff, M; Berger-Bächi, B (2001). Teicoplanin stress-selected mutations increasing sigma(B) activity in Staphylococcus aureus. Antimicrobial Agents and Chemotherapy, 45(6):1714-1720.

Abstract

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.

Abstract

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.

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58 citations in Web of Science®
59 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Medical Microbiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2001
Deposited On:30 Jul 2012 14:43
Last Modified:05 Apr 2016 15:47
Publisher:American Society for Microbiology (ASM)
ISSN:0066-4804
Free access at:PubMed ID. An embargo period may apply.
Publisher DOI:https://doi.org/10.1128/AAC.45.6.1714-1720.2001
PubMed ID:11353616

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