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Antimicrobial Agents and Chemotherapy, January 2000, p. 134-138, Vol. 44, No. 1
Departments of
Biology1 and
Chemistry,2 The Catholic University of
America, Washington, D.C. 20064; Department of Biology,
Immaculata College, Immaculata, Pennsylvania
193453; and Department of Chemistry and
Physics, University of the District of Columbia, Washington, D.C.
200084
Received 15 July 1999/Returned for modification 16 September
1999/Accepted 12 October 1999
To understand the chemical basis of action for the
PDR5-encoded multidrug resistance transporter of
Saccharomyces cerevisiae, we compared the relative
hypersensitivities of the wild-type (RW2802) and null mutant strains
toward a series of tri-n-alkyltin compounds. These
compounds differ from each other in a systematic fashion
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Copyright © 2000, American Society for Microbiology. All rights reserved.
Chemical Specificity of the PDR5
Multidrug Resistance Gene Product of Saccharomyces
cerevisiae Based on Studies with
Tri-n-Alkyltin Chlorides
either by
hydrocarbon chain length or by anion composition. Using
zone-of-inhibition and fixed-concentration assays, we found that the
ethyl, propyl, and butyl compounds are strong PDR5
substrates, whereas the methyl and pentyl compounds are weak. We
conclude that hydrophobicity and anion makeup are relatively
unimportant factors in determining whether a tri-n-alkyltin
compound is a good PDR5 substrate but that the dissociation
of the compound and the molecular size are significant.
*
Corresponding author. Mailing address: Department of
Biology, The Catholic University of America, Washington, DC 20064. Phone: (202) 319-5722. Fax: (202) 319-5721. E-mail:
Golin{at}cua.edu.
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