Nuclear but Not Mitochondrial DNA Involvement in Respiratory Complex I Defects Found in Senescence-Accelerated Mouse Strain, SAMP8

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  • IMANISHI Hirotake
    Graduate School of Life and Environmental Sciences, University of Tsukuba
  • YOKOTA Mutsumi
    Graduate School of Life and Environmental Sciences, University of Tsukuba Japan Society for the Promotion of Science (JSPS)
  • MORI Masayuki
    Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine
  • SHIMIZU Akinori
    Graduate School of Life and Environmental Sciences, University of Tsukuba
  • NAKADA Kazuto
    Graduate School of Life and Environmental Sciences, University of Tsukuba
  • HAYASHI Jun-Ichi
    Graduate School of Life and Environmental Sciences, University of Tsukuba

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  • Nuclear but not mitochondrial DNA involvement in respiratory complex 1 defects found in senescence-accelerated mouse strain, SAMP8

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Description

This study determined pathogenicity of an A11181G mtDNA mutation found in a senescence-accelerated mouse strain, SAMP8. The mutation was at a highly conserved site of the mt-Nd4 gene, which encodes one of the respiratory complex I subunits. The young SAMP8 expressed reduced complex I activity, which is controlled by both nuclear and mitochondrial DNA (mtDNA). To exclude the nuclear effects, we isolated transmitochondrial cybrids that share the same nuclear background, but possess mtDNA with or without the mutation. The cybrids showed normal respiratory function irrespective of whether their mtDNA possessed the mutation or not, suggesting that the A11181G mutation is not responsible for respiration defects found in SAMP8.<br>

Journal

  • Experimental Animals

    Experimental Animals 60 (4), 397-404, 2011

    Japanese Association for Laboratory Animal Science

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