Data supporting the results published in the paper entitled "Modulation of yeast Erg1 expression and terbinafine susceptibility by iron bioavailability"

The dataset is made available under the Open Database License. Any rights in individual contents of the database are licensed under the Database Contents License. Please, read the full ODbL 1.0 license text for the exact terms that apply. Users of the dataset are free to: Share: copy, distribute and use the database, either commercially or non-commercially. Create: produce derivative works from the database. Adapt: modify, transform and build upon the database. Under the following conditions: Attribution: You must attribute any public use of the database, or works produced from the database. For any use or redistribution of the database, or works produced from it, you must make clear to others the license of the original database. Share-Alike: If you publicly use any adapted version of this database, or works produced from an adapted database, you must also offer that adapted database under the ODbLErgosterol is a specific sterol component of yeast and fungal membranes. Its biosynthesis is one of the most effective targets for antifungal treatments. However, the emergent resistance to multiple sterol-based antifungal drugs emphasizes the need for new therapeutic approaches. The allylamine terbinafine, which selectively inhibits squalene epoxidase Erg1 within the ergosterol biosynthetic pathway, is mainly used to treat dermatomycoses, whereas its effectiveness in other fungal infections is limited. Given that ergosterol biosynthesis depends on iron as an essential cofactor, in this report we used the yeast Saccharomyces cerevisiae to investigate how iron bioavailability influences Erg1 expression and terbinafine susceptibility. We observed that both chemical and genetic depletion of iron decrease ERG1 expression, leading to an increase in terbinafine susceptibility. Deletion of either ROX1 transcriptional repressor or CTH1 and CTH2 post-transcriptional repressors of ERG1 expression led to an increase in Erg1 protein levels and terbinafine resistance. On the contrary, overexpression of CTH2 led to the opposite effect, lowering Erg1 levels and increasing terbinafine susceptibility. Although strain-specific particularities exist, opportunistic pathogenic strains of S. cerevisiae displayed a response similar to the laboratory strain. These data indicate that iron bioavailability and particular regulatory factors could be used to modulate susceptibility to terbinafine.This research was supported by grant PID2020-116940RB-I00 funded by MCIN/AEI/10.13039/501100011033 and predoctoral fellowship ACIF/2019/214 funded by “Generalitat Valenciana”.Peer reviewe