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


ABSTRACT: Candida albicans is a commensal yeast that inhabits the gastrointestinal tract of humans. The master regulator of the white-opaque transition WOR1 has been implicated in the adaptation to this commensal status. A proteomic analysis of cells overexpressing this transcription factor (WOR1OE) suggested an altered metabolism of carbon sources and a phenotypic analysis confirmed this alteration. The WOR1OE cells are deficient in using trehalose and xylose and are unable to use 2C sources, which is consistent with a reduction in the amount of Icl1, the isocitrate lyase enzyme. The icl1Δ/Δ mutants overexpressing WOR1 are deficient in the production of phloxine B positive cells, a main characteristic of opaque cells, a phenotype also observed in mating type hemizygous mtla1Δ icl1Δ/Δ cells, suggesting the involvement of Icl1 in the adaptation to the commensal state. In fact, icl1Δ/Δ cells have reduced fitness in mouse gastrointestinal tract as compared with essentially isogenic heterozygous ICL1/icl1Δ, but overproduction of WOR1 in an icl1Δ/Δ mutant does not restore fitness. These results implicate the glyoxylate shunt in the adaptation to commensalism of C. albicans by mechanisms that are partially independent of WOR1.

SUBMITTER: Vico SH 

PROVIDER: S-EPMC8304919 | biostudies-literature | 2021 Jun

REPOSITORIES: biostudies-literature

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The Glyoxylate Cycle Is Involved in White-Opaque Switching in <i>Candida albicans</i>.

Vico Susana Hidalgo SH   Prieto Daniel D   Monge Rebeca Alonso RA   Román Elvira E   Pla Jesús J  

Journal of fungi (Basel, Switzerland) 20210624 7


<i>Candida albicans</i> is a commensal yeast that inhabits the gastrointestinal tract of humans. The master regulator of the white-opaque transition <i>WOR1</i> has been implicated in the adaptation to this commensal status. A proteomic analysis of cells overexpressing this transcription factor (<i>WOR1<sup>OE</sup></i>) suggested an altered metabolism of carbon sources and a phenotypic analysis confirmed this alteration. The <i>WOR1<sup>OE</sup></i> cells are deficient in using trehalose and xy  ...[more]

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