Candida albicans strains adapted to the mouse gut are resistant to bile salts via a Flo8-dependent mechanism.

Candidaalbicans normally colonizes the human gastrointestinal tract as a commensal. Studying fungal factors involved in colonizing the mammalian gastrointestinal tract requires mouse models with altered microbiota. We have obtained strains of C.

Overexpression of the White Opaque Switching Master Regulator Wor1 Alters Lipid Metabolism and Mitochondrial Function in .

is a commensal yeast that inhabits the gastrointestinal tract of humans; increased colonization of this yeast in this niche has implicated the master regulator of the white-opaque transition, Wor1, by mechanisms not completely understood. We have addressed the role that this transcription factor has on commensalism by the characterization of strains overexpressing this gene. We show that overexpression causes an alteration of the total lipid content of the fungal cell and significantly alters the composition of structural and reserve molecular species lipids as determined by lipidomic analysis.

Identification of Clinical Isolates of with Increased Fitness in Colonization of the Murine Gut.

The commensal and opportunistic pathogen is an important cause of fungal diseases in humans, with the gastrointestinal tract being an important reservoir for its infections. The study of the mechanisms promoting the commensal state has attracted considerable attention over the last few years, and several studies have focused on the identification of the intestinal human mycobiota and the characterization of genes involved in its establishment as a commensal. In this work, we have barcoded 114 clinical isolates to identify strains with an enhanced fitness in a murine gastrointestinal commensalism model.

The Glyoxylate Cycle Is Involved in White-Opaque Switching in .

is a commensal yeast that inhabits the gastrointestinal tract of humans. The master regulator of the white-opaque transition has been implicated in the adaptation to this commensal status. A proteomic analysis of cells overexpressing this transcription factor () suggested an altered metabolism of carbon sources and a phenotypic analysis confirmed this alteration.

Deletion of the Gene in a Mutant Reverts Virulence in .

displays the ability to adapt to a wide variety of environmental conditions, triggering signaling pathways and transcriptional regulation. Sko1 is a transcription factor that was previously involved in early hypoxic response, cell wall remodeling, and stress response. In the present work, the role of mutant in o and studies was explored.