Project description:Transcript profiling from 3 biological replicates of C. albicans strains expressing PGA22 under the control of a tetracycline derivative-inducible promoter grown during 16h in the presence or absence of 50 µg/mL doxycycline (Dox)
Project description:Candida albicans is the most prevalent fungal pathogen of humans, causing a variety of diseases ranging from superficial mucosal infections to deep-seated systemic infections. Mucus, the gel that coats all wet epithelial surfaces, accommodates Candida albicans as part of the regular microbiome where C. albicans resides asymptomatically in healthy humans. Through a series of in vitro experiments combined with genome-wide transcriptional profiling, we show that mucin biopolymers, the main gel-forming constituents of mucus, induce a new oval-shaped morphology in C. albicans in which a range of genes related to adhesion, filamentation, and biofilm formation are down-regulated. We also show that corresponding phenotypes are suppressed, rendering Candida incapable of forming biofilms on a range of different synthetic surfaces and human epithelial cells. Our data suggests that mucins can manipulate Candida physiology and we hypothesize that they are key regulators for retaining Candida in the host-compatible, commensal state. 3 biological replicates grown in log phase in the presence and absence of mucin for 8 hours. Experiments were performed using RPMI 1640 (Gibco 31800-089) buffered with 165mM MOPS and supplemented with 0.2% NaHCO3 and 2% glucose with and without 0.5% mucin.
Project description:Presence of taurocholate (TC), a constituent of bile, confers resistance of Candida albicans to antifungals like Caspofungin and Amphotericin B. Transcriptional profiles in presence and absence of TC were compared to determine whether an upregulation of known resistance genes is responsible for this effect. No upregulation was found, and the resistance seemed to be rather based on a direct interaction of TC with the antifungals.
Project description:Transcriptional profiling of Candida albicans cells comparing control untreated C. albicans cells with sulfite-treated C. albicans cells. Sulfite is a toxic molecule that C. albicans encounters in its human host. Both wild type and ∆zcf2 mutant cells were used. The goal was to determine the effects of sulfite on C. albicans gene expression, and to determine which of the genes areZcf2-depedent.
Project description:The leucine CUG codon was reassigned to serine in the fungal pathogen Candida albicans. To clarify the biological role of this tuneable codon ambiguity on drug resistance, we evolved C. albicans strains that were engineered to mistranslate the CUG codon at constitutively elevated levels, in the presence and absence of the antifungal drug fluconazole. Elevated levels of mistranslation resulted in the rapid acquisition of resistance to fluconazole.
Project description:Transcriptional profiling of Candida albicans SC5314 comparing C. albicans grown in RPMI1640 or in RPMI1640 with 100ug/ml AAT. Goal was to determine the effects of AAT on global C. albicans gene expression.
