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(Received for publication, February 25, 1997, and in revised form, April 1, 1997)
From the For isolation of mouse mtDNA-less
(
Volume 272, Number 24,
Issue of June 13, 1997
pp. 15510-15515
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
,
,
,
,
,
Institute of Biological Sciences, University
of Tsukuba, Ibaraki 305, Japan, the § Department of
Pathology, Saitama Cancer Center Research Institute, Saitama 362, Japan, the ¶ Institut Gustave Roussy, 39 rue Camille Desmoulins,
94805 Villejuif Cédex, France, 
Rhone-Poulenc Rorer, Centre
de Recherche de Vitry-Alfortville 13, Quai Jules Guesde-BP14, 94403 Vitry Sur Seine, France, and the ** Department of Biochemistry,
Jichi Medical School, Tochigi 329-04, Japan
0) cell lines, we searched for various
antimitochondrial drugs that were expected to decrease the mtDNA
content and found that treatment with ditercalinium, an antitumor
bis-intercalating agent, was extremely effective for completely
excluding mtDNA in all the mouse cell lines we tested. The resulting
0 mouse cells were successfully used for trapping the
mtDNA of living nerve cells into dividing cultured cells by fusion of
the 0 cells with mouse brain synaptosomes, which
represent synaptic endings isolated from nerve cells. With neuronal
mtDNA obtained, all of the cybrid clones restored mitochondrial
translation activity similarly regardless of whether the mtDNA was
derived from young or aged mice, thus at least suggesting that defects
in mitochondrial genomes are not involved in the age-associated
mitochondrial dysfunction observed in the brain of aged mice.
Furthermore, we could trap a very small amount of a common 5823-base
pair deletion mutant mtDNA (
mtDNA5823) that was
detectable by polymerase chain reaction in the cybrid clones. As the
amount of mutant mtDNA with large scale deletions was expected to
increase during prolonged cultivation of the cybrids, these cells
should be available for establishment of mice containing the deletion
mutant mtDNA.
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