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Mitochondrial energy metabolism is required for lifespan extension by the spastic paraplegia-associated protein spartin
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Number of Authors: 18
2017 (English)In: Microbial Cell, ISSN 2311-2638, Vol. 4, no 12, 411-422 p.Article in journal (Refereed) Published
Abstract [en]

Hereditary spastic paraplegias, a group of neurodegenerative disorders, can be caused by loss-of-function mutations in the protein spartin. However, the physiological role of spartin remains largely elusive. Here we show that heterologous expression of human or Drosophila spartin extends chronological lifespan of yeast, reducing age-associated ROS production, apoptosis, and necrosis. We demonstrate that spartin localizes to the proximity of mitochondria and physically interacts with proteins related to mitochondrial and respiratory metabolism. Interestingly, Nde1, the mitochondrial external NADH dehydrogenase, and Pda1, the core enzyme of the pyruvate dehydrogenase complex, are required for spartin-mediated cytoprotection. Furthermore, spartin interacts with the glycolysis enhancer phospo-fructokinase-2,6 (Pfk26) and is sufficient to complement for PFK26-deficiency at least in early aging. We conclude that mitochondria-related energy metabolism is crucial for spartin's vital function during aging and uncover a network of specific interactors required for this function.

Place, publisher, year, edition, pages
2017. Vol. 4, no 12, 411-422 p.
Keyword [en]
SPG20, mitochondria, metabolism, respiration, pyruvate dehydrogenase, cell death, aging
National Category
Cell Biology
Identifiers
URN: urn:nbn:se:su:diva-150871DOI: 10.15698/mic2017.12.603ISI: 000417023400003PubMedID: 29234670OAI: oai:DiVA.org:su-150871DiVA: diva2:1172631
Available from: 2018-01-10 Created: 2018-01-10 Last updated: 2018-01-10Bibliographically approved

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Büttner, Sabrina
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Department of Molecular Biosciences, The Wenner-Gren Institute
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