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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 ODbL., Iron participates as an essential cofactor in the biosynthesis of critical cellular components, including DNA, proteins and lipids. The ergosterol biosynthetic pathway, which is an important target of antifungal treatments, depends on iron in four enzymatic steps. Our results in the model yeast Saccharomyces cerevisiae show that the expression of ergosterol biosynthesis (ERG) genes is tightly modulated by iron availability probably through the iron-dependent variation of sterol and heme levels. Whereas, the transcription factors Upc2 and Ecm22 are responsible for the activation of ERG genes upon iron deficiency, the heme-dependent factor Hap1 triggers their Tup1-mediated transcriptional repression. The combined regulation by both activating and repressing regulatory factors allows for the fine-tuning of ERG transcript levels along the progress of iron deficiency, avoiding the accumulation of toxic sterol intermediates and enabling efficient adaptation to rapidly changing conditions. The lack of these regulatory factors leads to changes in the yeast sterol profile upon iron-deficient conditions. Both environmental iron availability and specific regulatory factors should be considered in ergosterol antifungal treatments, This research was supported by grant PID2020-116940RB-I00 funded by MCIN/AEI/10.13039/501100011033 to Sergi Puig, and grants PID2020-120066RB-I00 funded by MCIN/AEI/10.13039/501100011033 and AICO/2020/086 by “Generalitat Valenciana” to Paula Alepuz. Tania Jordá was a recipient of a predoctoral fellowship ACIF/2019/214 funded by “Generalitat Valenciana”, and Marina Barba-Aliaga was a recipient of a predoctoral fellowship (FPU2017/03542) funded by MCIN/AEI/10.13039/501100011033 and by ESF-Investing in your future., Peer reviewed

Iron participates as an essential cofactor in the biosynthesis of critical cellular components, including DNA, proteins and lipids. The ergosterol biosynthetic pathway, which is an important target of antifungal treatments, depends on iron in four enzymatic steps. Our results in the model yeast Saccharomyces cerevisiae show that the expression of ergosterol biosynthesis (ERG) genes is tightly modulated by iron availability probably through the iron-dependent variation of sterol and heme levels. Whereas the transcription factors Upc2 and Ecm22 are responsible for the activation of ERG genes upon iron deficiency, the heme-dependent factor Hap1 triggers their Tup1-mediated transcriptional repression. The combined regulation by both activating and repressing regulatory factors allows for the fine-tuning of ERG transcript levels along the progress of iron deficiency, avoiding the accumulation of toxic sterol intermediates and enabling efficient adaptation to rapidly changing conditions. The lack of these regulatory factors leads to changes in the yeast sterol profile upon iron-deficient conditions. Both environmental iron availability and specific regulatory factors should be considered in ergosterol antifungal treatments., This research was supported by grant PID2020-116940RB-I00 funded by MCIN/AEI/10.13039/501100011033 to Sergi Puig, grants PID2020-120066RB-I00 funded by MCIN/AEI/10.13039/501100011033 and AICO/2020/086 by ‘Generalitat Valenciana’ to Paula Alepuz, and grant RED2018-102467-T funded by MCIN/AEI/10.13039/501100011033 to Sergi Puig and Paula Alepuz. Tania Jordá was a recipient of a predoctoral fellowship ACIF/2019/214 funded by ‘Generalitat Valenciana’, and Marina Barba-Aliaga was a recipient of a predoctoral fellowship (FPU2017/03542) funded by MCIN/AEI/10.13039/501100011033 and by ESF Investing in your future. The authors also acknowledge support of the publication fee by the CSIC Open Access Publication Support Initiative through its Unit of Information Resources for Research (URICI)., Peer reviewed

The eukaryotic translation initiation protein eIF5A is a highly conserved and essential factor that plays a critical role in different physiological and pathological processes including stress response and cancer. Different proteomic studies suggest that eIF5A may be a small ubiquitin-like modifier (SUMO) substrate, but whether eIF5A is indeed SUMOylated and how relevant is this modification for eIF5A activities are still unknown., Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature. Funding at the laboratory of CR is provided by Ministry of Science, Innovation and Universities and FEDER (BFU-2017-88880-P), (PID2021-126510NB-I00), and Xunta de Galicia (ED431G 2023/10). RS, SV and TLD are predoctoral fellows funded by Xunta de Galicia-Consellería de Cultura, Educación y Ordenación Universitaria (ED481A-2020/160, ED481A-2018/110, and ED481A-2018/042, respectively). AMR is a postdoctoral funded by Generalitat Valenciana (CIAPOS2021/117). MB is a predoctoral fellow funded by Banco Santander and University of Santiago de Compostela. RMT is a predoctoral fellow funded by Instituto de Investigación Sanitaria de Santiago de Compostela. The Blanco lab is supported by MCIN/AEI/https://doi.org/10.13039/501100011033 [PID2020-115472 GB-I00] and Xunta de Galicia/ FEDER ‘Una manera de hacer Europa’ [ED431C 2019/013]. RF lab is supported by Fondo de Investigación Sanitaria, ISCIII (PI20-00194). PA lab is supported by MCIN/AEI/https://doi.org/10.13039/501100011033 (PID2020-120066RB-I00) and by GVA CIAICO/2022/237. AMF is a predoctoral fellow funded by Asociación Española Contra el Cáncer (AECC APRO 2018). RB and JDS thank MCIN/AEI/https://doi.org/10.13039/501100011033 (PID2020-114178 GB-I00, CEX2021-001136-S). CR, RF and RB acknowledge SAF2017-90900-REDT support (UBIRed Program, Spain) and COST Action ProteoCure CA20113., Peer reviewed