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Objective: To determine whether low frequency mitochondrial DNA (mtDNA) mutations are pathogenic. Methods: We studied mice that express a proofreading-deficient mitochondrial DNA polymerase in the heart and develop cardiac mtDNA mutations. Results: At 4 weeks of age, when point mutation levels had risen to on average two per mitochondrial genome, these mice developed severe dilated cardiomyopathy...
With age, mitochondrial DNA mutations and oxidative stress increase, leading to the hypothesis that the production of reactive oxygen species causes the pathogenic effects of mitochondrial DNA mutations. We tested this hypothesis using transgenic mice that develop cardiomyopathy due to the accumulation of mitochondrial DNA mutations specifically in the heart. Surprisingly, the mechanism of pathogenesis...
Transgenic mice having rapid accumulation of mitochondrial DNA (mtDNA) mutations specifically in the heart were created. These mice contained a transgene encoding a proofreading-deficient, mouse mitochondrial DNA polymerase (pol γ) driven by the promoter for the cardiac-specific α-myosin heavy chain. Starting shortly after birth greater than 95% of all pol γ mRNA in the heart was transgene derived;...
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