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Journal of Bacteriology, October 2002, p. 5810-5813, Vol. 184, No. 20
0021-9193/02/$04.00+0 DOI: 10.1128/JB.184.20.5810-5813.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
K. M. Winterberg,
L. McDowell,
M. B. Schmid,|| and J. M. Buysse
Essential Therapeutics, Inc., Mountain View, California 94043
Received 22 April 2002/ Accepted 15 July 2002
The yycF1(Ts) mutation in Staphylococcus aureus conferred hypersensitivity to macrolide-lincosamide-streptogramin B (MLSB) antibiotics on strains either containing or lacking ermB. The overexpression of the S. aureus Ssa protein restored the yycF1 mutant to wild-type levels of susceptibility. Inactivation of ssa in an unmutagenized strain dramatically reduced ermB-based resistance. Conditional loss of function or expression of ssa in the yycF1 mutant is proposed to result in the observed hypersensitivity to MLSB antibiotics.
Present address: Silicon Genetics, Inc., Redwood City, CA 94063.
Present address: University of Wisconsin, Department of Biochemistry, Madison, WI 53706-1544.
Present address: Antibacterial Molecular Sciences, Pfizer Global Research and Development, Ann Arbor, MI 48105.
|| Present address: Affinium Pharmaceuticals, Inc., Toronto, Ontario M5J 1V6, Canada.
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