TY - JOUR
T1 - The filamentation pathway controlled by the Efg1 regulator protein is required for normal biofilm formation and development in Candida albicans
AU - Ramage, Gordon
AU - VandeWalle, Kacy
AU - López-Ribot, José L.
AU - Wickes, Brian L.
N1 - Funding Information:
This work was supported by Grant ATP 3659-0080 from the Texas Higher Education Coordinating Board (Advance Technology Program, Biomedicine). J.L.L.-R. is the recipient of a New Investigator Award in Molecular Pathogenic Mycology from the Burroughs Wellcome Fund. We thank Dr. Gerald Fink for providing C. albicans mutant strains used in this work. We also thank Peggy Miller (Dept. of Pathology) for assistance in SEM experiments.
PY - 2002/8/27
Y1 - 2002/8/27
N2 - 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 (Δcph1, Δefg1, Δhst7, and Δcst20) and compared these mutants to wild-type strains to determine whether filamentation is an integral factor for biofilm formation. Scanning electron microscopy revealed that Δcph1, Δhst7 and Δcst20 mutants were able to filament and form structured biofilms displaying three-dimensional architecture similar to those formed by wild-type strains. However, Δefg1 and Δcph1/Δefg1 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.
AB - 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 (Δcph1, Δefg1, Δhst7, and Δcst20) and compared these mutants to wild-type strains to determine whether filamentation is an integral factor for biofilm formation. Scanning electron microscopy revealed that Δcph1, Δhst7 and Δcst20 mutants were able to filament and form structured biofilms displaying three-dimensional architecture similar to those formed by wild-type strains. However, Δefg1 and Δcph1/Δefg1 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.
KW - Biofilm
KW - Candida albicans
KW - Dimorphism
KW - Hyphae
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U2 - 10.1016/S0378-1097(02)00853-4
DO - 10.1016/S0378-1097(02)00853-4
M3 - Article
C2 - 12204378
AN - SCOPUS:0037183376
VL - 214
SP - 95
EP - 100
JO - FEMS Microbiology Letters
JF - FEMS Microbiology Letters
SN - 0378-1097
IS - 1
ER -