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Abstract
The transcriptional regulator Wor1 has been shown to induce the GUT transition, an environmentally triggered process that increases the fitness of Candida albicans in the mouse gastrointestinal tract. We have developed strains where the expression of this gene is driven from the strong and tightly regulated tetracycline promoter. These cells retain the main characteristics reported for GUT cells albeit they show defects in the initial stages of colonization. They also show a differential colonization along the gastrointestinal tract compared to isogenic strains, which is probably caused by their susceptibility to bile salts. We also show that WOR1 overexpressing cells have an altered metabolic activity, as revealed by a different susceptibility to inhibitors of respiration, and an enhanced adhesion to the mouse mucosa. We propose that this may contribute to their long-term favored ability to colonize the gastrointestinal tract.
Highlights
The fungus Candida albicans is a frequent colonizer of the human gastrointestinal and female vaginal tract
Therapies directed against the associated genes and proteins or the processes involved may lead to the eradication of C. albicans from the gut or to restrict its presence as a “domesticated” commensal, both of potential usefulness in the prevention of candidiasis
We chose in this study the doxycycline regulated promoter (Park and Morschhauser, 2005) to express WOR1, as it represents a strong promoter widely used in C. albicans research and, most importantly, because of its ability to regulate gene expression in vivo
Summary
The fungus Candida albicans is a frequent colonizer of the human gastrointestinal and female vaginal tract. It is estimated that more than 50% of human individuals without an underlying pathology are colonized with this fungus and this value may be higher as colonization is highly dependent on the physiological status of the patient. Alteration of the host defenses facilitates the access of the microbe to other non-canonical body locations causing severe diseases called candidiasis. These conditions are, frequently, life threatening and may result in mortalities as high as ≈50% (Gudlaugsson et al, 2003). Therapies directed against the associated genes and proteins or the processes involved may lead to the eradication of C. albicans from the gut or to restrict its presence as a “domesticated” commensal, both of potential usefulness in the prevention of candidiasis
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