Abstract:Hypoxia is encountered frequently by Candida albicans during systemic infection of the human host. We tested if hypoxia allows biofilm formation by C. albicans, which is a major cause for the perseverance and antifungal resistance of its infections. Using an in vitro biofilm system we unexpectedly discovered that several positive regulators of biofilm formation during normoxia including Tec1, Ace2, Czf1, Och1 and Als3 had no or little influence for biofilm development during hypoxia, irrespective of carbon dioxide levels, indicating that C. albicans biofilm pathways differ depending on oxygen levels. In contrast, the Efg1 and Flo8 regulators were required for both normoxic and hypoxic biofilm formation. To explore the role of Efg1 during hypoxic and/or biofilm growth we determined transcriptomal kinetics following release of EFG1 expression by a tet-on system. During hypoxia, Efg1 rapidly induced all major classes of genes known to be associated with normoxic biofilm formation, including genes involved in glycolysis, sulfur metabolism and antioxidative/peroxisomal activities, as well as genes for iron uptake. The results suggest that hypoxic adaptation mediated by the Efg1/Flo8 regulators is required even during normoxic biofilm development, while hypoxic biofilm formation in deep tissues or in organs may generate foci of C. albicans infections.

Status: Published Type: Journal Article PubMed ID: 19346360

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