Abstract
Candida albicans is the most important fungal pathogen of humans. Biofilm is a common phenomenon of natural microbe communities, in which cells attach and grow on a biotic or an anbiotic surface, and has been proved to be highly related to virulence of pathogens. In C. albicans, biofilm formation shows a significant consequence for human health and contributes to implanted medical device-associated infections and drug resistance. The formation of C. albicans biofilm is a complex process that involves different cell phenotypes including cell adhesion, cell-cell interaction, yeast-hyphae morphogenesis and extracellular matrix secretion. Mss11p is a transcription factor and controls flocculation and biofilm formation of the model yeast, Saccharomyces cerevisiae. According to the high similarity between C. albicans and S. cerevisiae, In an effort to search the homolog of ScMSS11 in Candida genome database, orf19.6309 is identified as CaMSS11. To examine the functions of C. albicans MSS11 gene, I have knocked-out the genes by the SAT1 flipper method. In the comparisons between wild type and CaMSS11 mutant strains, the mutant strains cause some phenotypic defects that are similar to that of ScMSS11 deletion strains, including cell morphogenesis, invasion, biofilm formation. The difference in biofilm formation ability is the most significant phenotype. The ability of adhering to surface showed no difference between different strains, while the susceptibility of CaMSS11 deletion strains to cell wall integrity interference reagents is different from wild type (SC5314). Moreover, cell to cell interaction is weaker in the mutant strains and the deletion of CaMSS11 gene does not affect virulence in a mouse model of systemic infection. Together, the results suggest that CaMSS11 is the homolog of ScMSS11 and it plays an important role in Candida biofilm maturation