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Post-Transcriptional Regulation of the Sef1 Transcription Factor Controls the Virulence of Candida albicans in Its Mammalian Host
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Post-Transcriptional Regulation of the Sef1 Transcription Factor Controls the Virulence of Candida albicans in Its Mammalian Host
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Journal Article
Post-Transcriptional Regulation of the Sef1 Transcription Factor Controls the Virulence of Candida albicans in Its Mammalian Host
2012
Overview
The yeast Candida albicans transitions between distinct lifestyles as a normal component of the human gastrointestinal microbiome and the most common agent of disseminated fungal disease. We previously identified Sef1 as a novel Cys(6)Zn(2) DNA binding protein that plays an essential role in C. albicans virulence by activating the transcription of iron uptake genes in iron-poor environments such as the host bloodstream and internal organs. Conversely, in the iron-replete gastrointestinal tract, persistence as a commensal requires the transcriptional repressor Sfu1, which represses SEF1 and genes for iron uptake. Here, we describe an unexpected, transcription-independent role for Sfu1 in the direct inhibition of Sef1 function through protein complex formation and localization in the cytoplasm, where Sef1 is destabilized. Under iron-limiting conditions, Sef1 forms an alternative complex with the putative kinase, Ssn3, resulting in its phosphorylation, nuclear localization, and transcriptional activity. Analysis of sfu1 and ssn3 mutants in a mammalian model of disseminated candidiasis indicates that these post-transcriptional regulatory mechanisms serve as a means for precise titration of C. albicans virulence.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Candida albicans - metabolism
/ Candida albicans - pathogenicity
/ Core Binding Factor Alpha 1 Subunit - biosynthesis
/ Core Binding Factor Alpha 1 Subunit - genetics
/ Cyclin-Dependent Kinases - genetics
/ Cyclin-Dependent Kinases - metabolism
/ Fungal Proteins - metabolism
/ Gene Expression Regulation, Fungal - physiology
/ Humans
/ Iron
/ Kinases
/ Mammals
/ Medicine
/ Multiprotein Complexes - genetics
/ Multiprotein Complexes - metabolism
/ Mutation
/ Proteins
/ Rodents
/ Yeasts
