Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Breitenbach 2012 Abstract Bioblast

From Bioblast
Breitenbach M, Mattanovich D, Marx H, Sauer M, Ralser M, Rinnerthaler M, Grabner C, Dawes I (2012) Roles of mitochondria in aging and in energy metabolism. Mitochondr Physiol Network 17.12.

Link: MiPNet17.12 Bioblast 2012 - Open Access

Breitenbach M, Mattanovich D, Marx H, Sauer M, Ralser M, Rinnerthaler M, Grabner C, Dawes I (2012)

Event: Bioblast 2012

Michael Breitenbach

A yeast deletion mutant in the gene AFO1, coding for a mitochondrial ribosomal protein, confers respiratory deficiency, resistance to several oxidants, a 60% increased replicative lifespan, and very surprisingly, rapid growth on glucose and a highly efficient energy metabolism. The gene defect induces loss of the mitochondrial genome. We showed that the effect of the mutation on lifespan is independent of the retrograde response, and defines a longevity signaling mechanism from the mitochondria to the nuclear/cytoplasmic gene expression system which depends on the presence of an intact TOR1 gene and glucose as a carbon source. The mutant displays an extraordinarily low level of oxygen radicals. We show that this mutation grows rapidly and produces ethanol and biomass on glucose with a kinetics comparable to wild type, in stark contrast to a bona fide ethidium bromide induced rho-zero strain, which grows slowly. The growth phenotypes were shown to be the same in two quite different genetic backgrounds, one of them completely prototrophic. Transcriptome and metabolic analysis of wild type and mutant confirms metabolic similarity of the two strains and points to futile metabolic cycles in the bona fide rho-zero strain, which could be reponsible for slow growth of the rho-zero strain. Taken together, the phenotype of the mutant points to the fact that slow growth of rho-zero strains is not caused by slow and inefficient production of ATP, as is often maintained in the textbooks, but is rather a metabolic regulatory phenomenon. It is the intention of this contribution to aid understanding of the role of oxidative stress response and the mitochondria in the mother cell-specific aging process.

  1. Laun P, Pichova A, Madeo F, Fuchs J, Ellinger A, Kohlwein S, Dawes I, Fröhlich KU, Breitenbach M (2001) Mol Microbiol 39: 1166-1173.
  2. Heeren G, Rinnerthaler M, Laun P, von Seyerl P, Kössler S, Klinger H, Hager M, Bogengruber E, Jarolim S, Simon-Nobbe B, Schüller C, Carmona-Gutierrez D, Breitenbach-Koller L, Mück C, Jansen-Dürr P, Criollo A, Kroemer G, Madeo F, Breitenbach M (2009) The mitochondrial ribosomal protein of the large subunit, Afo1p, determines cellular longevity through mitochondrial back-signaling via TOR1. Aging (Albany NY) 1: 622-636 Open Access
  3. Rinnerthaler M, Büttner S, Laun P, Heeren G, Felder TK, Klinger H, Weinberger M, Stolze K, Grousl T, Hasek J, Benada O, Frydlova I, Klocker A, Simon-Nobbe B, Jansko B, Breitenbach-Koller H, Eisenberg T, Gourlay CW, Madeo F, Burhans WC, Breitenbach M (2012) Yno1p/Aim14p, a NADPH-oxidase ortholog, controls extramitochondrial reactive oxygen species generation, apoptosis, and actin cable formation in yeast. Proc Natl Acad Sci U S A 109: 8658-8663. Open Access

Keywords: Aging, Yeast, TOR1, Oxidative stress

O2k-Network Lab: AT Salzburg Breitenbach M

Labels: Pathology: Aging;senescence  Stress:Oxidative stress;RONS  Organism: Fungi 

Regulation: ATP production, Substrate 

Affiliations and author contributions

Michael Breitenbach (1), Diethard Mattanovich (2), Hans Marx (2), Michael Sauer (2), Markus Ralser (3), Mark Rinnerthaler (1), Christian Grabner (1), Ian Dawes (4)

(1) Dept. Cell Biology, University of Salzburg, Austria; Email: [email protected]

(2) Dept. Biotechnology, University of Life Sciences, Vienna, Austria

(3) Cambridge Systems Biology Center and Dept. Biochemistry, University of Cambridge, UK

(4) School of Biochemistry and Molecular Genetics, University of NSW, Sydney, Australia