Mitochondrial transcription factor A is necessary for mtDNA maintance and embryogenesis in mice
Copyright policy )Mitochondrial transcription factor A is necessary for mtDNA maintance and embryogenesis in mice
The regulation of mitochondrial DNA (mtDNA) expression is crucial for mitochondrial biogenesis during development and differentiation. We have disrupted the mouse gene for mitochondrial transcription factor A (Tfam; formerly known as m-mtTFA) by gene targetting of loxP-sites followed by cre-mediated excision in vivo. Heterozygous knockout mice exhibit reduced mtDNA copy number and respiratory chain deficiency in heart. Homozygous knockout embryos exhibit a severe mtDNA depletion with abolished oxidative phosphorylation. Mutant embryos proceed through implantation and gastrulation, but die prior to embryonic day (E)10.5. Thus, Tfam is the first mammalian protein demonstrated to regulate mtDNA copy number in vivo and is essential for mitochondrial biogenesis and embryonic development.
- Stanford University United States
- French Institute of Health and Medical Research France
- University of California, San Francisco United States
- Howard Hughes Medical Institute United States
Mice, Knockout, Heterozygote, Fetal Growth Retardation, Integrases, Gene Dosage, High Mobility Group Proteins, Gene Expression Regulation, Developmental, Nuclear Proteins, Heart, DNA, Mitochondrial, Mitochondria, DNA-Binding Proteins, Mitochondrial Proteins, Mice, Mutation, Animals, Female, Embryo Implantation, Phosphorylation, Fetal Death
Mice, Knockout, Heterozygote, Fetal Growth Retardation, Integrases, Gene Dosage, High Mobility Group Proteins, Gene Expression Regulation, Developmental, Nuclear Proteins, Heart, DNA, Mitochondrial, Mitochondria, DNA-Binding Proteins, Mitochondrial Proteins, Mice, Mutation, Animals, Female, Embryo Implantation, Phosphorylation, Fetal Death
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