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. 2022 Feb 8;13:750. doi: 10.1038/s41467-022-28358-w

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a The architecture of DdCBE monomers targeting m.9576 G (C₁₂) and m.9577 G (C₁₃). The DNA specificity is provided by TALE domains. In each experiment, different DddA_tox splits are used (G1397 or G1333, purple) to achieve editing of “TC” sites. MTS SOD2 mitochondrial targeting sequence from superoxide dismutase 2, UGI uracil glycosylase inhibitor, L-strand or (L) light mtDNA strand, H-strand or (H) heavy mtDNA strand. b The details and possible outcomes of m.9576 G (C₁₂) and m.9577 G (C₁₃) editing. The purple box indicates the desired editing sites; other potential editing sites are indicated in purple. c The structural model of mouse complex I with indicated MT-ND3 subunit (red). The inset shows the location of MT-ND3 p.G40K mutation on the evolutionary conserved MT-ND3 loop.