Interaction theory of mammalian mitochondria

We generated mice with deletion mutant mtDNA by its introduction from somat ic cells into mouse zygotes. Expressions of disease phenotypes are limited to tissues expressing mitochondrial dysfunction. Considering that all these mice share the same nuclear background, these observations suggest that ac cumulation of the mutant mtDNA and resultant expressions of mitochondrial. dysfunction are responsible for expression of disease phenotypes. On the ot her hand, mitochondrial dysfunction and expression of clinical abnormalitie s were not observed until the mutant mtDNA accumulated predominantly. This protection is due to the presence of extensive and continuous interaction b etween exogenous mitochondria from cybrids and recipient mitochondria from embryos. Thus, we would like to propose a new hypothesis on mitochondrial b iogenesis, interaction theory of mitochondria: mammalian mitochondria excha nge genetic contents, and thus lost the individuality and function as a sin gle dynamic cellular Unit. (C) 2001 Academic Press.