Consequences of lysine auxotrophy for Candida albicans adherence and biofilm formation

Abstract

A number of factors are known to be involved in Candida albicans virulence although biofilm development on the surfaces of indwelling medical devices is considered to promote superficial or systemic disease. Accordingly to previously reported up-regulation of saccharopine and acetyllysine in biofilm cells and activation of the lysine biosynthesis/degradation pathway we investigated the consequences of Candida albicans lysine auxotrophy on adhesion to host tissues and biofilm formation. Our data indicate that mutant strains lysD21/lysD22, defective in homocitrate synthase and lysD4, homoaconitase activity (two first a-aminoadipate pathway enzymes) are able to adhere to mouse embryonic fibroblast cell line (NIH/3T3) with the same extent as control strain SC5314. On the other hand auxotrophic mutant strains development on mouse fibroblasts monolayers was significantly reduced up to 5h of infection. Although invasion into human-derived oral epithelial cells was unaltered, both mutant strains formed significantly different biofilm architecture and demonstrated diminished viability during long term biofilm propagation.