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Mitochondrial DNA editing in mice with DddA-TALE fusion deaminases

Cited 27 time in Web of Science Cited 31 time in Scopus
Issue Date
2021-02
Citation
Nature Communications, Vol.12 No.1, p. 1190
Abstract
DddA-derived cytosine base editors (DdCBEs), composed of the split interbacterial toxin DddA(tox), transcription activator-like effector (TALE), and uracil glycosylase inhibitor (UGI), enable targeted C-to-T base conversions in mitochondrial DNA (mtDNA). Here, we demonstrate highly efficient mtDNA editing in mouse embryos using custom-designed DdCBEs. We target the mitochondrial gene, MT-ND5 (ND5), which encodes a subunit of NADH dehydrogenase that catalyzes NADH dehydration and electron transfer to ubiquinone, to obtain several mtDNA mutations, including m.G12918A associated with human mitochondrial diseases and m.C12336T that incorporates a premature stop codon, creating mitochondrial disease models in mice and demonstrating a potential for the treatment of mitochondrial disorders. Split DddA-derived base editors fused to TALEs enable mitochondrial DNA editing. Here the authors demonstrate their use in mouse embryos with germline transmission.
ISSN
2041-1723
URI
https://hdl.handle.net/10371/179116
DOI
https://doi.org/10.1038/s41467-021-21464-1
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