Gene-specific transcriptional activation by the AtrR factor requires a conserved C-terminal domain.

Unlabelled: Treatment of fungal infections associated with the filamentous fungus is becoming more problematic as this organism is developing resistance to the main chemotherapeutic drug at an increasing rate. Azole drugs represent the current standard-of-care in the treatment of aspergillosis with this drug class acting by inhibiting a key step in the biosynthesis of the fungal sterol ergosterol. Azole compounds block the activity of the lanosterol α-14 demethylase, encoded by the gene.

Loss of a conserved C-terminal region of the AtrR transcriptional regulator leads to a gene-specific defect in target gene expression.

Treatment of fungal infections associated with the filamentous fungus is becoming more problematic as this organism is developing resistance to the main chemotherapeutic drug at an increasing rate. Azole drugs represent the current standard-of-care in treatment of aspergillosis with this drug class acting by inhibiting a key step in biosynthesis of the fungal sterol ergosterol. Azole compounds block the activity of the lanosterol α-14 demethylase, encoded by the gene.

Biochemical Identification of a Nuclear Coactivator Protein Required for AtrR-Dependent Gene Regulation in Aspergillus fumigatus.

Azole drugs represent the primary means of treating infections associated with the filamentous fungal pathogen Aspergillus fumigatus. A central player in azole resistance is the ZnCys zinc cluster-containing transcription factor AtrR. This factor stimulates expression of both the gene, which encodes the azole drug target enzyme, as well as an ATP-binding cassette transporter-encoding gene called ().

Ifu5, a WW domain-containing protein interacts with Efg1 to achieve coordination of normoxic and hypoxic functions to influence pathogenicity traits in Candida albicans.

Hypoxic adaptation pathways, essential for Candida albicans pathogenesis, are tied to its transition from a commensal to a pathogen. Herein, we identify a WW domain-containing protein, Ifu5, as a determinant of hypoxic adaptation that also impacts normoxic responses in this fungus. Ifu5 activity supports glycosylation homeostasis via the Cek1 mitogen-activated protein kinase-dependent up-regulation of PMT1, under normoxia.

Sef1-Regulated Iron Regulon Responds to Mitochondria-Dependent Iron-Sulfur Cluster Biosynthesis in .

Iron homeostasis mechanisms allow the prime commensal-pathogen to cope with the profound shift in iron levels in the mammalian host. The regulators, Sef1 and Sfu1 influence activation and repression of genes required for iron uptake and acquisition by inducing the expression of iron regulon genes in iron-deplete conditions and inactivating them in iron-replete condition. Our study for the first time shows that coordinates the activation of the iron regulon with the mitochondrial use of iron for Fe-S cluster biosynthesis, a cellular process that is connected to cellular iron metabolism.