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- W2556590524 abstract "Mitochondrial DNA (mtDNA) often exists in a state of heteroplasmy, in which mutant mtDNA co-exists in cells with wild-type mtDNA. High frequencies of pathogenic mtDNA result in maternally inherited diseases; maternally and somatically acquired mutations also accumulate over time and contribute to diseases of ageing. Reducing heteroplasmy is therefore a therapeutic goal and in vivo models in post-mitotic tissues are needed to facilitate these studies. Here we describe a transgene-based model of a heteroplasmic lethal mtDNA deletion (mtDNAΔ) in adult Drosophila muscle. Stimulation of autophagy, activation of the PINK1/parkin pathway or decreased levels of mitofusin result in a selective decrease in mtDNAΔ. Decreased levels of mitofusin and increased levels of ATPIF1, an inhibitor of ATP synthase reversal-dependent mitochondrial repolarization, result in a further decrease in mtDNAΔ levels. These results show that an adult post-mitotic tissue can be cleansed of a deleterious genome, suggesting that therapeutic removal of mutant mtDNA can be achieved." @default.
- W2556590524 created "2016-11-30" @default.
- W2556590524 creator A5026877316 @default.
- W2556590524 creator A5036252424 @default.
- W2556590524 creator A5062611456 @default.
- W2556590524 creator A5091827717 @default.
- W2556590524 date "2016-11-14" @default.
- W2556590524 modified "2023-09-23" @default.
- W2556590524 title "Selective removal of deletion-bearing mitochondrial DNA in heteroplasmic Drosophila" @default.
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- W2556590524 doi "https://doi.org/10.1038/ncomms13100" @default.
- W2556590524 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5114534" @default.
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