Ura-status-dependent adhesion of Candida albicans mutants

FEMS Microbiol Lett. 2001 Nov 13;204(2):323-8. doi: 10.1111/j.1574-6968.2001.tb10905.x.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Candida albicans / genetics*
  • Candida albicans / growth & development
  • Candida albicans / pathogenicity
  • Candida albicans / physiology*
  • Cell Adhesion
  • Collagen
  • Drug Combinations
  • Epithelial Cells / microbiology
  • Fungal Proteins / genetics*
  • Fungal Proteins / metabolism*
  • Gene Deletion*
  • Humans
  • Laminin
  • Mouth Mucosa / cytology
  • Mouth Mucosa / microbiology
  • Proteoglycans
  • Virulence


  • Drug Combinations
  • Fungal Proteins
  • Laminin
  • Proteoglycans
  • matrigel
  • Collagen