Excess copper causes repression of global translation in Saccharomyces cerevisiae
- 1Departament de Bioquímica i Biología Molecular, Universitat de València
- 2Departamento de Biotecnología, Instituto de Agroquímica y Tecnología de Alimentos (IATA), Consejo Superior de Investigaciones Científicas (CSIC)
Abstract
Copper is an essential cofactor for numerous metabolic pathways; however, excess intracellular copper is cytotoxic. In this study, we investigated the consequences of deregulated Cu+ uptake mediated by the high-affinity copper transporter Ctr1 in the model yeast Saccharomyces cerevisiae. Constitutive expression of a carboxy-terminally truncated Ctr1 variant, CTR1(300), resulted in elevated intracellular copper levels, increased oxidative stress, and reduced oxygen consumption, likely due to impairment of iron-sulfur cluster-containing proteins. Notably, CTR1(300)-expressing cells exhibited a pronounced repression of global protein synthesis at very low copper concentrations, a phenotype that was recapitulated in wild-type cells when exposed to higher copper levels. These findings reveal that excessive Cu+ accumulation negatively impacts cellular respiration and translation, identifying protein synthesis as a sensitive target of copper toxicity.
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BibTeX
@article{andresborderia2026excess,
title = {{Excess copper causes repression of global translation in Saccharomyces cerevisiae}},
author = {Amparo Andrés-Bordería and Antonia M. Romero and Raquel Sorribes-Dauden and Lola Peñarrubia and María T. Martínez-Pastor and Sergi Puig and Ana Perea-García},
journal = {Scientific Reports},
year = {2026},
month = jun,
doi = {10.1038/s41598-026-56882-y},
url = {https://doi.org/10.1038/s41598-026-56882-y},
note = {CC BY},
}
RIS
TY - JOUR
TI - Excess copper causes repression of global translation in Saccharomyces cerevisiae
AU - Amparo Andrés-Bordería
AU - Antonia M. Romero
AU - Raquel Sorribes-Dauden
AU - Lola Peñarrubia
AU - María T. Martínez-Pastor
AU - Sergi Puig
AU - Ana Perea-García
PY - 2026
DA - 2026/06/01
JO - Scientific Reports
DO - 10.1038/s41598-026-56882-y
UR - https://doi.org/10.1038/s41598-026-56882-y
AB - Copper is an essential cofactor for numerous metabolic pathways; however, excess intracellular copper is cytotoxic. In this study, we investigated the consequences of deregulated Cu+ uptake mediated by the high-affinity copper transporter Ctr1 in the model yeast Saccharomyces cerevisiae. Constitutive expression of a carboxy-terminally truncated Ctr1 variant, CTR1(300), resulted in elevated intracellular copper levels, increased oxidative stress, and reduced oxygen consumption, likely due to impairment of iron-sulfur cluster-containing proteins. Notably, CTR1(300)-expressing cells exhibited a pronounced repression of global protein synthesis at very low copper concentrations, a phenotype that was recapitulated in wild-type cells when exposed to higher copper levels. These findings reveal that excessive Cu+ accumulation negatively impacts cellular respiration and translation, identifying protein synthesis as a sensitive target of copper toxicity.
SN - 2045-2322
ER -