The filamentation pathway controlled by the Efg1 regulator protein is required for normal biofilm formation and development in Candida albicans
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Updated: Sep 29, 2026

Use of In Vivo Imaging to Screen for Morphogenesis Phenotypes in Candida albicans Mutant Strains During Active Infection in a Mammalian Host
Published on: October 12, 2022
Gordon Ramage1, Kacy VandeWalle, José L López-Ribot
1Department of Microbiology, Mail Code 7850, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, 78229-3900, USA.
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 (Deltacph1, Deltaefg1, Deltahst7, and Deltacst20) and compared these mutants to wild-type strains to determine whether filamentation is an integral factor for biofilm formation. Scanning electron microscopy revealed that Deltacph1, Deltahst7 and Deltacst20 mutants were able to filament and form structured biofilms displaying three-dimensional architecture similar to those formed by wild-type strains. However, Deltaefg1 and Deltacph1/Deltaefg1 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.
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