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Antimicrobial Agents and Chemotherapy, February 1999, p. 240-245, Vol. 43, No. 2
Institute for Medical Microbiology,
University of Zürich, CH-8028 Zürich,
Switzerland,1 and
Department of
Microbiology, Hiroshima University School of Dentistry, Kasumi
1-2-3, Minami-ku, Hiroshima City, Hiroshima 734-8553, Japan2
Received 10 August 1998/Returned for modification 2 October
1998/Accepted 12 November 1998
The Staphylococcus aureus phosphoglucosamine mutase
gene glmM was shown to be the last gene of a
three-cistron operon, orf1-orf2-glmM. One
transcriptional start was identified upstream of orf1, and a second start producing a monocistronic transcript was identified upstream of glmM. Disruption of glmM abolished
GlmM production, decreased methicillin resistance, and resulted in
teicoplanin hypersusceptibility without affecting the production of the
endogenous penicillin-binding proteins and PBP 2'. Complementation of
the glmM mutation by the complete glmM
operon restored both methicillin resistance and normal teicoplanin
susceptibility. In contrast, a highly methicillin-resistant suppressor
mutant obtained by selection for growth in the presence of methicillin
remained GlmM deficient and teicoplanin hypersusceptible. The
suppressor mutation was not linked to the glmM operon but
was correlated with decreased autolysis and increased production of a
49-kDa protein, suggesting that there is an alternative
pathway for glucosamine-1-phosphate synthesis in S. aureus.
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
glmM Operon and Methicillin-Resistant
glmM Suppressor Mutants in Staphylococcus
aureus

*
Corresponding author. Mailing address: Institute for
Medical Microbiology, University of Zürich, Gloriastr. 32, P.O.
Box, CH8028 Zürich, Switzerland. Phone: 41-1 634 26 50. Fax: 41-1 634 49 06. E-mail: bberger{at}immv.unizh.ch.
Present address: Curtin University of Technology, P.O.
Box U1987, Perth 6001, Western Australia.
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