2000 Fiscal Year Final Research Report Summary
Generation and application of mtDNA knockout mice models of aging
| Project/Area Number |
10832001
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
老化(加齢)
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| Research Institution | University of Tsukuba |
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Principal Investigator |
HAYASHI Jun-ichi University of Tsukuba, Institute of Biological Sciences Professor, 生物科学系, 教授 (60142113)
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| Project Period (FY) |
1998 – 2000
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| Keywords | Mouse mtDNA / mtDNA Mutation / Mitochondrial transfer / Aging model mice / mitochondrial tRNA |
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| Research Abstract |
Mice possessing pathogenic mutant mitochondrial DNA (mtDNA) would provide ideal systems for studying exactly how mutant mtDNAs are transmitted and distributed in tissues resulting in expression of mitochondrial diseases, but no effective procedures are available for their generation. Isolation of mtDNA-less (ρ^0) mouse cells enabled us to trap mouse mutant mtDNAs that had accumulated in somatic tissues into mtDNA repopulated ρ^0 cells (cybrids). We could isolate respiration-deficient cybrids with a deletion mutant mtDNA and introduce it into fertilized eggs. The mutant mtDNA was transmitted maternally, and its accumulation induced mitochondrial dysfunction in various tissues. Moreover, most of these mice unexpectedly died as a consequence of renal failure, suggesting the involvement of mtDNA mutations in the pathogeneses of new diseases.
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[Publications] Yuko Aomi, Chu-Shih Chen, Kazuto Nakada, Sayaka Ito, Kotoyo Isobe, Haruka Murakami, Shin-ya Kuno, Masato Tawata, Rumiko Matsuoka, Hidehiro Mizusawa, and Jun-Ichi Hayashi.: "Cytoplasmic transfer of platelet mtDNA from elderly patients with Parkinson's disease to mtDNA-less HeLa cells restores complete mitochondrial respiratory function."Biochem. Biophys. Res. Commun.. 280. 265-273 (2001)
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