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Antimicrobial Agents and Chemotherapy, December 2004, p. 4505-4512, Vol. 48, No. 12
0066-4804/04/$08.00+0 DOI: 10.1128/AAC.48.12.4505-4512.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
CaNdt80 Is Involved in Drug Resistance in Candida albicans by Regulating CDR1
Chia-Geun Chen,1,2
Yun-Liang Yang,3
Hsin-I Shih,3
Chia-Li Su,2 and
Hsiu-Jung Lo2*
Graduate Institute of Life Sciences, National Defense Medical Center,1
Division of Clinical Research, National Health Research Institutes, Taipei,2
Department of Biological Science and Technology, National Chiao Tung University, Hsinchu, Taiwan, Republic of China.3
Received 29 July 2004/
Returned for modification 18 August 2004/
Accepted 23 August 2004
Overexpression of CDR1, an efflux pump, is one of the major mechanisms contributing to drug resistance in Candida albicans. CDR1 p-lacZ was constructed and transformed into a Saccharomyces cerevisiae strain so that the lacZ gene could be used as the reporter to monitor the activity of the CDR1 promoter. Overexpression of CaNDT80, the C. albicans homolog of S. cerevisiae NDT80, increases the ß-galactosidase activity of the CDR1 p-lacZ construct in S. cerevisiae. Furthermore, mutations in CaNDT80 abolish the induction of CDR1 expression by antifungal agents in C. albicans. Consistently, the Candt80/Candt80 mutant is also more susceptible to antifungal drugs than the wild-type strain. Thus, the gene for CaNdt80 may be the first gene among the regulatory factors involved in drug resistance in C. albicans whose function has been identified.
* Corresponding author. Mailing address: Division of Clinical Research, National Health Research Institutes, 128, Yen-Chiu-Yuan Rd., Section 2, Taipei 11529, Taiwan, Republic of China. Phone: 886-2-2652-4095. Fax: 886-2-2789-0254. E-mail: hjlo{at}nhri.org.tw.
Antimicrobial Agents and Chemotherapy, December 2004, p. 4505-4512, Vol. 48, No. 12
0066-4804/04/$08.00+0 DOI: 10.1128/AAC.48.12.4505-4512.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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Copyright © 2004 by the American Society for Microbiology. All rights reserved.