The filamentation pathway controlled by the Efg1 regulator protein is required for normal biofilm formation and development in Candida albicans

Abstract

Candida albicans biofilms are structured microbial communities composed of a mixture of yeast cells and hyphal elements, suggesting a pivotal role for the dimorphic switch in the development of biofilms. We have used C. albicans mutants defective in genes involved in filamentation (Δ cph1, Δ efg1, Δ hst7, and Δ cst20) and compared these mutants to wild-type strains to determine whether filamentation is an integral factor for biofilm formation. Scanning electron microscopy revealed that Δ cph1, Δ hst7 and Δ cst20 mutants were able to filament and form structured biofilms displaying three-dimensional architecture similar to those formed by wild-type strains. However, Δ efg1 and Δ cph1/Δ efg1 mutants were unable to filament and did not form biofilms, but rather sparse monolayers of loosely attached elongated, rod-like, cells. Antimicrobial susceptibility testing showed intrinsic resistance of all mutant strains to fluconazole and amphotericin B when attached to the surface of biomaterials. These results suggest that hyphal formation is pivotal for biofilm development in C. albicans. However, the sessile lifestyle associated with adherent cells confers antifungal resistance, regardless of coherent biofilm formation.