Author
Listed:
- Satomi Miwa
(Institute for Ageing and Health, Newcastle University)
- Howsun Jow
(Centre for Integrated Systems Biology of Ageing and Nutrition, Newcastle University)
- Karen Baty
(Newcastle University Protein and Proteome Analysis, Devonshire Building, Devonshire Terrace)
- Amy Johnson
(Institute for Ageing and Health, Newcastle University)
- Rafal Czapiewski
(Institute for Ageing and Health, Newcastle University)
- Gabriele Saretzki
(Institute for Ageing and Health, Newcastle University)
- Achim Treumann
(Newcastle University Protein and Proteome Analysis, Devonshire Building, Devonshire Terrace)
- Thomas von Zglinicki
(Institute for Ageing and Health, Newcastle University)
Abstract
Mitochondrial function is an important determinant of the ageing process; however, the mitochondrial properties that enable longevity are not well understood. Here we show that optimal assembly of mitochondrial complex I predicts longevity in mice. Using an unbiased high-coverage high-confidence approach, we demonstrate that electron transport chain proteins, especially the matrix arm subunits of complex I, are decreased in young long-living mice, which is associated with improved complex I assembly, higher complex I-linked state 3 oxygen consumption rates and decreased superoxide production, whereas the opposite is seen in old mice. Disruption of complex I assembly reduces oxidative metabolism with concomitant increase in mitochondrial superoxide production. This is rescued by knockdown of the mitochondrial chaperone, prohibitin. Disrupted complex I assembly causes premature senescence in primary cells. We propose that lower abundance of free catalytic complex I components supports complex I assembly, efficacy of substrate utilization and minimal ROS production, enabling enhanced longevity.
Suggested Citation
Satomi Miwa & Howsun Jow & Karen Baty & Amy Johnson & Rafal Czapiewski & Gabriele Saretzki & Achim Treumann & Thomas von Zglinicki, 2014.
"Low abundance of the matrix arm of complex I in mitochondria predicts longevity in mice,"
Nature Communications, Nature, vol. 5(1), pages 1-12, September.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms4837
DOI: 10.1038/ncomms4837
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