Mitochondrial DNA editing in mice with DddA-TALE fusion deaminases

Hyunji Lee, Seonghyun Lee, Gayoung Baek, Annie Kim, Beum-Chang Kang, Huiyun Seo and Jin-Soo Kim ()
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Hyunji Lee: Center for Genome Engineering, Institute for Basic Science
Seonghyun Lee: Center for Genome Engineering, Institute for Basic Science
Gayoung Baek: Center for Genome Engineering, Institute for Basic Science
Annie Kim: Center for Genome Engineering, Institute for Basic Science
Beum-Chang Kang: Center for Genome Engineering, Institute for Basic Science
Huiyun Seo: Center for Genome Engineering, Institute for Basic Science
Jin-Soo Kim: Center for Genome Engineering, Institute for Basic Science

Nature Communications, 2021, vol. 12, issue 1, 1-6

Abstract: Abstract DddA-derived cytosine base editors (DdCBEs), composed of the split interbacterial toxin DddAtox, 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.

Date: 2021
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DOI: 10.1038/s41467-021-21464-1

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