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Journal of Bacteriology, January 2000, p. 76-80, Vol. 182, No. 1
Department of Biology, Georgia State
University, Atlanta, Georgia 30303
Received 5 August 1999/Accepted 5 October 1999
Saccharomyces cerevisiae, along with other eukaryotes,
is resistant to tetracyclines. We found that deletion of
SOD1 (encoding Cu/Zn superoxide dismutase) rendered
S. cerevisiae hypersensitive to oxytetracycline (OTC): a
sod1
0021-9193/0/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.
Copper/Zinc-Superoxide Dismutase Is Required for
Oxytetracycline Resistance of Saccharomyces
cerevisiae

mutant exhibited a >95% reduction in
colony-forming ability at an OTC concentration of 20 µg
ml
1, whereas concentrations of up to 1,000 µg
ml
1 had no effect on the growth of the wild type. OTC
resistance was restored in the sod1
mutant by
complementation with wild-type SOD1. The effect of OTC
appeared to be cytotoxic and was not evident in a ctt1
(cytosolic catalase) mutant or in the presence of tetracycline. SOD1 transcription was not induced by OTC, suggesting that
constitutive SOD1 expression is sufficient for wild-type
OTC resistance. OTC uptake levels in wild-type and sod1
strains were similar. However, lipid peroxidation and protein oxidation
were both enhanced during exposure of the sod1
mutant,
but not the wild type, to OTC. We propose that Sod1p protects S. cerevisiae against a mode of OTC action that is dependent on
oxidative damage.
*
Corresponding author. Mailing address: Department of
Biology, Georgia State University, University Plaza, Atlanta, GA 30303. Phone: (404) 651-0912. Fax: (404) 651-2509. E-mail:
biosva{at}panther.gsu.edu.
Present address: Emory University School of Medicine, Atlanta, GA 30322.
Present address: Boston University School of Medicine, Boston, MA.
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