Publications
Detailed Information
Mitochondrial DNA editing in mice with DddA-TALE fusion deaminases
Cited 85 time in
Web of Science
Cited 84 time in Scopus
- Authors
- Issue Date
- 2021-02-19
- Publisher
- Nature Publishing Group
- 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
- Files in This Item:
- There are no files associated with this item.
- Appears in Collections:
Item View & Download Count
Items in S-Space are protected by copyright, with all rights reserved, unless otherwise indicated.