Abstract
Gene disruptions in the diploid opportunistic human fungal pathogen Candida albicans are usually created using multiple rounds of targeted integration called the 'ura-blaster' method. Resulting heterozygous and homozygous null mutants can be auxotrophic (Ura-) or prototrophic (Ural) for uracil biosynthesis. Here we demonstrate that the Ura-status of otherwise isogenic mutants affected the adhesion of C albicans. Moreover the effect of Ura-status on adhesion was also dependent on the null mutant background, the nature of the underlying surface and the carbon source for growth. Therefore the Ura-status is not neutral in determining adhesive properties of C albicans mutants that are generated via the ura-blaster protocol. (C) 2001 Federation of European Microbiological Societies. Published by Elsevier Science B.V. All rights reserved.
Original language | English |
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Pages (from-to) | 323-328 |
Number of pages | 5 |
Journal | FEMS Microbiology Letters |
Volume | 204 |
Issue number | 2 |
DOIs | |
Publication status | Published - Nov 2001 |
Keywords
- adhesion
- gene disruption
- medical mycology
- mutagenesis
- Candida albicans
- DIFFERENT CARBON-SOURCES
- BUCCAL EPITHELIAL-CELLS
- AUXOTROPHIC MUTANTS
- GENE DISRUPTION
- EXPERIMENTAL INFECTIONS
- PROTEINASE GENES
- ADHERENCE
- VIRULENCE
- STRAINS
- GROWTH