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Induced expression of the Candida albicans multidrug resistance gene CDR1 in response to fluconazole and other antifungals
Author(s) -
Hernáez María Luisa,
Gil Concha,
Pla Jesús,
Nombela César
Publication year - 1998
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/(sici)1097-0061(19980430)14:6<517::aid-yea250>3.0.co;2-d
Subject(s) - biology , candida albicans , azole , cycloheximide , microbiology and biotechnology , corpus albicans , open reading frame , multiple drug resistance , gene , gene expression , efflux , fluconazole , drug resistance , genetics , peptide sequence , protein biosynthesis , antifungal
The Candida albicans CDR1 gene encodes a member of the ABC‐type family of multidrug transporters which has been shown to be involved in azole resistance. Using an in‐frame gene fusion between the CDR1 open reading frame and the green fluorescent protein allele yEGFP3 , an optimized derivative for its use in C. albicans , we show here how the CDR1‐yEGFP3 gene expression is induced in response to azoles as well as to other structurally unrelated drugs like cycloheximide. Moderate increases were observed for calcofluor, canavanine, 5′‐fluorcytosine, cilofungin and caffeine, while no induction was found for the antifungals benomyl and amphotericin B or hydrogen peroxide at subinhibitory concentrations. The use of confocal microscopy enabled us to localize the Cdr1p fusion protein at the cell periphery, thus suggesting a cytoplasmic membrane localization. These results suggest deregulation of CDR1 gene as a putative mechanism for the generation of azole resistance in this clinically important pathogenic fungus. © 1998 John Wiley & Sons, Ltd.