| Résumé | Prostaglandins are hormone-like chemicals involved in the inflammatory response and in defense against pathogens. We investigated the effect of extracellular prostaglandin E2 (PGE2) on the human fungal pathogen Candida albicans. Transcriptional analysis of C. albicans treated with PGE2 indicated differential expression of genes involved in alternative carbon source catabolism, and showed repression of genes encoding components of both the translational machinery and the homolog of Saccharomyces cerevisiae Mac1 regulon needed for iron uptake. Prostaglandin-mediated repression of the Mac1 regulon required the Tup1p transcriptional regulator, and did not occur in hyphal cells. Analysis of the promoter of the Mac1 regulon component FRE7 revealed a well-conserved palindromic Mac1p binding site that was critical for expression of a downstream reporter. To identify elements other than Tup1 that are involved in regulation of the Mac1 regulon, we screened a C. albicans transcription factor mutant library with this FRE7 promoter fused to a lacZ reporter. Oaf1p, Stp4p, Azf1p, and Cas1p mutants showed moderate enhancement of reporter expression. Azf1p and Cas1p were shown to be transducers of the PGE2 dependent signaling pathway |
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