Changes of mitochondrial ultrastructure and function during ageing in mice and Drosophila
Tobias Brandt,
Arnaud Mourier,
Luke S Tain,
Linda Partridge,
Nils-Göran Larsson,
Werner Kühlbrandt
Affiliations
Tobias Brandt
Department of Structural Biology, Max-Planck-Institute of Biophysics, Frankfurt am Main, Germany
Arnaud Mourier
Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Cologne, Germany; Institut de Biochimie et Génétique Cellulaires UMR 5095, Université de Bordeaux, Bordeaux, France; CNRS, Institut de Biochimie et Génétique Cellulaires UMR 5095, Bordeaux, France
Luke S Tain
Department of Biological Mechanisms of Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany
Linda Partridge
Department of Biological Mechanisms of Ageing, Max Planck Institute for Biology of Ageing, Cologne, Germany; Institute of Healthy Ageing, Department of Genetics, Evolution, and Environment, University College London, London, United Kingdom
Nils-Göran Larsson
Department of Mitochondrial Biology, Max Planck Institute for Biology of Ageing, Cologne, Germany; Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden
Ageing is a progressive decline of intrinsic physiological functions. We examined the impact of ageing on the ultrastructure and function of mitochondria in mouse and fruit flies (Drosophila melanogaster) by electron cryo-tomography and respirometry. We discovered distinct age-related changes in both model organisms. Mitochondrial function and ultrastructure are maintained in mouse heart, whereas subpopulations of mitochondria from mouse liver show age-related changes in membrane morphology. Subpopulations of mitochondria from young and old mouse kidney resemble those described for apoptosis. In aged flies, respiratory activity is compromised and the production of peroxide radicals is increased. In about 50% of mitochondria from old flies, the inner membrane organization breaks down. This establishes a clear link between inner membrane architecture and functional decline. Mitochondria were affected by ageing to very different extents, depending on the organism and possibly on the degree to which tissues within the same organism are protected against mitochondrial damage.
