Data on the role of iba57p in free Fe2+ release and O2∙− generation in Saccharomyces cerevisiae
Mauricio Gomez-Gallardo,
Luis A. Sánchez,
Alma L. Díaz-Pérez,
Christian Cortés-Rojo,
Jesús Campos-García
Affiliations
Mauricio Gomez-Gallardo
Lab. de Biotecnología Microbiana, Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mich., Mexico
Luis A. Sánchez
Lab. de Biotecnología Microbiana, Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mich., Mexico
Alma L. Díaz-Pérez
Lab. de Biotecnología Microbiana, Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mich., Mexico
Christian Cortés-Rojo
Lab. de Bioquímica, Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mich., Mexico
Jesús Campos-García
Lab. de Biotecnología Microbiana, Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Mich., Mexico; Correspondence to: Lab. de Biotecnología Microbiana, Instituto de Investigaciones Químico Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Edif. B-3, Ciudad Universitaria, 58030 Morelia, Michoacán, Mexico.
The related study has confirmed that in Saccharomyces cerevisiae, iba57 protein participates in maturation of the [2Fe–2S] cluster into the Rieske protein, which plays important roles in the conformation and functionality of mitochondrial supercomplexes III/IV in the electron transport chain (Sánchez et al., 2018) [1]. We determined in S. cerevisiae the effects of mutation in the IBA57 gene on reactive oxygen species (ROS) and iron homeostasis. Flow cytometry and confocal microscopy analyses showed an increased generation of ROS, correlated with free Fe2+ release in the IBA57 mutant yeast. Data obtained support that a dysfunction in the Rieske protein has close relationship between ROS generation and free Fe2+ content, and which is possible that free Fe2+ release mainly proceeds from [Fe–S] cluster-containing proteins.
