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BioMed Research International
Volume 2014 (2014), Article ID 101286, 12 pages
Research Article

Alteration of ROS Homeostasis and Decreased Lifespan in S. cerevisiae Elicited by Deletion of the Mitochondrial Translocator FLX1

1Istituto di Biomembrane e Bioenergetica, CNR, Via Amendola 165/A, 70126 Bari, Italy
2Dipartimento di Bioscienze, Biotecnologie e Biofarmaceutica, Università degli Studi di Bari “A. Moro”, Via Orabona 4, 70126 Bari, Italy
3Institute of Molecular Biosciences, Goethe University Frankfurt, Max-von-Laue Straße 9, 60438 Frankfurt am Main, Germany
4Dipartimento di Fisica, Via P. Giuria 1, 10125 Torino, Italy

Received 31 January 2014; Revised 20 March 2014; Accepted 1 April 2014; Published 8 May 2014

Academic Editor: Dina Bellizzi

Copyright © 2014 Teresa Anna Giancaspero et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This paper deals with the control exerted by the mitochondrial translocator FLX1, which catalyzes the movement of the redox cofactor FAD across the mitochondrial membrane, on the efficiency of ATP production, ROS homeostasis, and lifespan of S. cerevisiae. The deletion of the FLX1 gene resulted in respiration-deficient and small-colony phenotype accompanied by a significant ATP shortage and ROS unbalance in glycerol-grown cells. Moreover, the strain showed H2O2 hypersensitivity and decreased lifespan. The impaired biochemical phenotype found in the strain might be justified by an altered expression of the flavoprotein subunit of succinate dehydrogenase, a key enzyme in bioenergetics and cell regulation. A search for possible cis-acting consensus motifs in the regulatory region upstream SDH1-ORF revealed a dozen of upstream motifs that might respond to induced metabolic changes by altering the expression of Flx1p. Among these motifs, two are present in the regulatory region of genes encoding proteins involved in flavin homeostasis. This is the first evidence that the mitochondrial flavin cofactor status is involved in controlling the lifespan of yeasts, maybe by changing the cellular succinate level. This is not the only case in which the homeostasis of redox cofactors underlies complex phenotypical behaviours, as lifespan in yeasts.