Interaction theory of mammalian mitochondria.

Abstract

We generated mice with deletion mutant mtDNA by its introduction from somatic 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 accumulation of the mutant mtDNA and resultant expressions of mitochondrial dysfunction are responsible for expression of disease phenotypes. On the other hand, mitochondrial dysfunction and expression of clinical abnormalities were not observed until the mutant mtDNA accumulated predominantly. This protection is due to the presence of extensive and continuous interaction between exogenous mitochondria from cybrids and recipient mitochondria from embryos. Thus, we would like to propose a new hypothesis on mitochondrial biogenesis, interaction theory of mitochondria: mammalian mitochondria exchange genetic contents, and thus lost the individuality and function as a single dynamic cellular unit.

• Authors: K Nakada, K Inoue, J Hayashi
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 288 Issue 4 Pg. 743-6 (Nov 09 2001) ISSN: 0006-291X [Print] United States
• PMID: 11688969 (Publication Type: Journal Article)
• Copyright: Copyright 2001 Academic Press.

Chemical References

• DNA, Mitochondrial

Topics

• Animals
• Cell Nucleus (genetics)
• Congenital Abnormalities (genetics, pathology)
• Cytoplasm (genetics, transplantation)
• DNA, Mitochondrial (genetics, metabolism)
• Extrachromosomal Inheritance (genetics)
• Mice
• Mitochondria (genetics, pathology, physiology, transplantation)
• Mitochondrial Diseases (genetics, metabolism, pathology)
• Models, Biological
• Models, Genetic
• Mutation (genetics)
• Phenotype
• Rats
• Recombination, Genetic (genetics)
• Zygote (metabolism, pathology)