期刊
GENETICS
卷 167, 期 4, 页码 1855-1861出版社
GENETICS SOCIETY AMERICA
DOI: 10.1534/genetics.103.021287
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Mitochondrial disease model mice, mitomice, were created using zygotes of B6mtspr strain mice carrying mitochondrial DNA (mtDNA) from Mus spretus as recipients of exogenous mitochondria carrying wildtype and a deletion mutant mtDNA (DeltamtDNA) of M. musculus domesticus. In these experiments, mtDNAs from different mouse species were used for identification of exo- and endogenous wild-type mtDNAs in the mitomice. Results showed transmission of exogenous DeltamtDNA, but not exogenous wild-type mtDNA, of M. m. domesticus to following generations through the female germ line. Complete elimination of exogenous wild-type mtDNA would be due to stochastic segregation, whereas transmission of exogenous DeltamtDNA would be due to its smaller size leading to a propagational advantage. Tissues in mitomice of the F-3 generation carrying exogenous DeltamtDNA showed protection from respiration defects until DeltamtDNA accumulated predominantly. This protection from expression of mitochondrial dysfunction was attained with the help of endogenous wild-type mtDNA of M. spretus, since mitomice did not possess exogenous wild-type mtDNA of M. m. domesticus. These observations provide unambiguous evidence for the presence of interaction between exogenous mitochondria carrying DeltamtDNA and endogenous mitochondria carrying M spretus wild-type mtDNA.
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