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  Increased Total mtDNA Copy Number Cures Male Infertility Despite Unaltered mtDNA Mutation Load

Jiang, M., Kauppila, T. E. S., Motori, E., Li, X., Atanassov, I., Folz-Donahue, K., et al. (2017). Increased Total mtDNA Copy Number Cures Male Infertility Despite Unaltered mtDNA Mutation Load. Cell Metab, 26(2), 429-436 e4. doi:10.1016/j.cmet.2017.07.003.

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Datensatz-Permalink: https://hdl.handle.net/21.11116/0000-0001-5909-2 Versions-Permalink: https://hdl.handle.net/21.11116/0000-0001-590A-1
Genre: Zeitschriftenartikel

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externe Referenz:
https://www.ncbi.nlm.nih.gov/pubmed/28768180 (beliebiger Volltext)
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 Urheber:
Jiang, M.1, Autor
Kauppila, T. E. S.1, Autor
Motori, E.1, Autor
Li, X.1, Autor
Atanassov, I.1, Autor
Folz-Donahue, K.1, Autor
Bonekamp, N. A.1, Autor
Albarran-Gutierrez, S.1, Autor
Stewart, J. B.1, Autor
Larsson, N. G.1, Autor
Affiliations:
1Max Planck Institute for Biology of Ageing, Max Planck Society, Joseph-Stelzmann-Str. 9b, D-50931 Cologne, DE, ou_1942284              

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Schlagwörter: Polga Tfam infertility mitochondria mtDNA mutator mouse spermatogenesis
 Zusammenfassung: Mutations of mtDNA cause mitochondrial diseases and are implicated in age-associated diseases and aging. Pathogenic mtDNA mutations are often present in a fraction of all mtDNA copies, and it has been widely debated whether the proportion of mutant genomes or the absolute number of wild-type molecules determines if oxidative phosphorylation (OXPHOS) will be impaired. Here, we have studied the male infertility phenotype of mtDNA mutator mice and demonstrate that decreasing mtDNA copy number worsens mitochondrial aberrations of spermatocytes and spermatids in testes, whereas an increase in mtDNA copy number rescues the fertility phenotype and normalizes testes morphology as well as spermatocyte proteome changes. The restoration of testes function occurs in spite of unaltered total mtDNA mutation load. We thus demonstrate that increased copy number of mtDNA can efficiently ameliorate a severe disease phenotype caused by mtDNA mutations, which has important implications for developing future strategies for treatment of mitochondrial dysfunction.

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 Datum: 2017
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: -
 Identifikatoren: Anderer: 28768180
DOI: 10.1016/j.cmet.2017.07.003
ISSN: 1932-7420 (Electronic)1550-4131 (Linking)
 Art des Abschluß: -

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Titel: Cell Metab
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 26 (2) Artikelnummer: - Start- / Endseite: 429 - 436 e4 Identifikator: -