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Oxidative Medicine and Cellular Longevity
Volume 2013 (2013), Article ID 636287, 13 pages
Research Article

Maintenance of Mitochondrial Morphology by Autophagy and Its Role in High Glucose Effects on Chronological Lifespan of Saccharomyces cerevisiae

1School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia
2Department of Genetics, University of Salzburg, Hellbrunnerstrare 34, 5020 Salzburg, Austria

Received 13 May 2013; Accepted 21 June 2013

Academic Editor: Joris Winderickx

Copyright © 2013 May T. Aung-Htut 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.

Supplementary Material

The supplementary Tables S1 and S2 include data relative to: the volatile components produced by growth of cells to stationary phase in media containing different concentrations of glucose. The Supplementary Figures illustrate: the effects of mutations in mitochondrial fission/fusion on mitochondrial morphology (Fig. S1); the effect on mitochondrial morphology of mutating or inhibiting the TOR pathway (Figs. S1 and S2); the effects of compounds leading to intracellular acidification on mitochondrial morphology (Fig. S4); and, the intracellular pH of cells grown in media containing different concentrations of glucose (Fig S5).

Table S1 provides an estimation of the concentrations of the main volatile metabolites (ethanol, acetic acid and 2,3-butanediol in conditioned media from cells grown in SC medium containing 0.4%, 2% or 4% glucose.

Table S2 gives the intracellular acetate concentration in the wild-type and mutant cells grown for 72 h in SC medium containing different concentrations of glucose.

Figure S1 illustrates the mitochondrial morphology in cells of the wild type and dnm1, fis1 and fzo1 mutants defective in mitochondrial fission and fusion.

Figure S2 illustrates that deletion of TOR1 protects cells against mitochondrial fragmentation.

Figure S3 shows that rapamycin treatment also prevents mitochondrial fragmentation.

Figure S4 Acetic acid, benzoic acid and 2,4-DNP triggered mitochondrial fragmentation in S. cerevisiae.

Figure S5 gives the intracellular pH of cells grown in different concentrations of glucose.

  1. Supplementary Materials