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  Low-level mitochondrial heteroplasmy modulates DNA replication, glucose metabolism and lifespan in mice

Hirose, M., Schilf, P., Gupta, Y., Zarse, K., Künstner, A., Fähnrich, A., et al. (2018). Low-level mitochondrial heteroplasmy modulates DNA replication, glucose metabolism and lifespan in mice. Scientific Reports, 8(1): 5872. doi:10.1038/s41598-018-24290-6.

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Item Permalink: http://hdl.handle.net/21.11116/0000-0001-9BFD-4 Version Permalink: http://hdl.handle.net/21.11116/0000-0001-9BFE-3
Genre: Journal Article

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 Creators:
Hirose, Misa, Author
Schilf, Paul, Author
Gupta, Yask, Author
Zarse, Kim, Author
Künstner, Axel, Author
Fähnrich, Anke, Author
Busch, Hauke, Author
Yin, Junping1, Author              
Wright, Marvin N., Author
Ziegler, Andreas, Author              
Vallier, Marie1, Author              
Belheouane, Meriem1, Author              
Baines, John F.1, Author              
Tautz, Diethard2, Author              
Johann, Kornelia, Author
Oelkrug, Rebecca, Author
Mittag, Jens, Author
Lehnert, Hendrik, Author
Othman, Alaa, Author
Jöhren, Olaf, Author
Schwaninger, Markus, AuthorPrehn, Cornelia, AuthorAdamski, Jerzy, AuthorShima, Kensuke, AuthorRupp, Jan, AuthorHäsler, Robert, AuthorFuellen, Georg, AuthorKöhling, Rüdiger, AuthorRistow, Michael, AuthorIbrahim, Saleh M., Author more..
Affiliations:
1Guest Group Evolutionary Genomics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445638              
2Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society, ou_1445635              

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 Abstract: Mutations in mitochondrial DNA (mtDNA) lead to heteroplasmy, i.e., the intracellular coexistence of wild-type and mutant mtDNA strands, which impact a wide spectrum of diseases but also physiological processes, including endurance exercise performance in athletes. However, the phenotypic consequences of limited levels of naturally arising heteroplasmy have not been experimentally studied to date. We hence generated a conplastic mouse strain carrying the mitochondrial genome of an AKR/J mouse strain (B6-mtAKR) in a C57BL/6 J nuclear genomic background, leading to >20% heteroplasmy in the origin of light-strand DNA replication (OriL). These conplastic mice demonstrate a shorter lifespan as well as dysregulation of multiple metabolic pathways, culminating in impaired glucose metabolism, compared to that of wild-type C57BL/6 J mice carrying lower levels of heteroplasmy. Our results indicate that physiologically relevant differences in mtDNA heteroplasmy levels at a single, functionally important site impair the metabolic health and lifespan in mice.

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Language(s): eng - English
 Dates: 2017-10-032018-03-292018-04-122018
 Publication Status: Published in print
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Title: Scientific Reports
  Abbreviation : Sci. Rep.
Source Genre: Journal
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Publ. Info: London, UK : Nature Publishing Group
Pages: - Volume / Issue: 8 (1) Sequence Number: 5872 Start / End Page: - Identifier: ISSN: 2045-2322
CoNE: https://pure.mpg.de/cone/journals/resource/2045-2322