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 (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.

Status: Published Type: Journal article PubMed ID: 11731143

• To find other papers on a gene and topic, click on the colored ball in the appropriate box.
  displays other papers with information about that topic for that gene.
  displays other papers in CGD that are associated with that topic.
  The topic is addressed in these papers but does not describe a specific gene or chromosomal feature.


• To go to the Locus page for a gene, click on the gene name.