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Generation of mice with mitochondrial dysfunction by introducing mouse mtDNA carrying a deletion into zygotes

Inoue, Kimiko, Nakada, Kazuto, Ogura, Atsuo, Isobe, Kotoyo, Goto, Yu-ichi, Nonaka, Ikuya, Hayashi, Jun-Ichi·2000·Nature Genetics
DOI 10.1038/82826
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Abstract

Mice carrying mitochondrial DNA (mtDNA) with pathogenic mutations would provide a system in which to study how mutant mtDNAs are transmitted and distributed in tissues, resulting in expression of mitochondrial diseases. However, no effective procedures are available for the generation of these mice. Isolation of mouse cells without mtDNA (rho0) enabled us to trap mutant mtDNA that had accumulated in somatic tissues into rho0 cells repopulated with mtDNA (cybrids). We isolated respiration-deficient cybrids with mtDNA carrying a deletion and introduced this mtDNA into fertilized eggs. The mutant mtDNA was transmitted maternally, and its accumulation induced mitochondrial dysfunction in various tissues. Moreover, most of these mice died because of renal failure, suggesting the involvement of mtDNA mutations in the pathogeneses of new diseases.

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  • Efforts using enucleated human cybrids and mouse pronuclear cells to generate mouse models for the 4.7 kb 'common deletion' failed to achieve progeny beyond F3.

    “Efforts using enucleated human cybrids and mouse pronuclear cells to generate mouse models for the 4.7 kb “common deletion” that overtakes a rising number of postmitotic cells with age failed to achieve progeny beyond F3 [148].”

    From The Mitochondrial Genome in Aging and Disease and the Future of Mitochondrial Therapeutics (2022) · cites this paper as [148]

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Metadata

Authors
Inoue, K., Nakada, K., Ogura, A., Isobe, K., Goto, Y.-I., Nonaka, I., & Hayashi, J.-I.
Venue
Nature Genetics
Publisher
Springer Science and Business Media LLC
Published
2000-10
Volume
26
Issue
2
Pages
176-181
ISSN
  • 1061-4036
  • 1546-1718
DOI
10.1038/82826
Cited by
333
References
3
Language
en
Licence
www.springer.com/tdm (tdm)

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