Ura-status-dependent adhesion of Candida albicans mutants.
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 (Ura(+)) 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.
Bain
J M
JM
Department of Molecular and Cell Biology, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, UK.
Stubberfield
C
C
Gow
N A
NA
D002176:Candida albicans / Q000235:genetics* / Q000254:growth & development / Q000472:pathogenicity / Q000502:physiology*; D002448:Cell Adhesion; D003094:Collagen; D004338:Drug Combinations; D004847:Epithelial Cells / Q000382:microbiology; D005656:Fungal Proteins / Q000235:genetics* / Q000378:metabolism*; D017353:Gene Deletion; D006801:Humans; D007797:Laminin; D009061:Mouth Mucosa / Q000166:cytology / Q000382:microbiology; D011509:Proteoglycans; D014774:Virulence
D004338:Drug Combinations; D005656:Fungal Proteins; D007797:Laminin; D011509:Proteoglycans; C059485:matrigel; D003094:Collagen