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. 2021 Oct 19;7(1):95.
doi: 10.1038/s41421-021-00325-7.

Precision modeling of mitochondrial disease in rats via DdCBE-mediated mtDNA editing

Affiliations

Precision modeling of mitochondrial disease in rats via DdCBE-mediated mtDNA editing

Xiaolong Qi et al. Cell Discov. .
No abstract available

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1. Mitochondrial disorder modeling by DdCBE in rat.
a Representative sequence chromatograms of G7755A (Left) and G14098A (Right) founder rats. Target sites are indicated by red arrows. b Frequencies of G-to-A conversion at G7755 (Blue dots) and G14098 (Red dots) in founder rats. c Frequencies of mtDNA G-to-A conversion of offspring from G14098A #7 founder. The red dot indicates founder, black dots indicate F1 offspring. d Measuring distance (Left) and speed (Right) by open field test. e Evaluation of motor coordination by Rotarod test. f Measuring grip strength by Grip Strength Test. gm Echocardiography analysis of wild-type rats and edited F1 males. The tests include a snapshot of M-mode of echocardiography (g), left ventricular (LV) diameter at end-diastole and end-systole (LVIDD, LVIDS) (h, i), LV anterior wall thickness at end-diastole and end-systole (LVAWD, LVAWS) (j, k), LV ejection fraction (LVEF) (l), and LV percent fractional shortening (LVFS) (m). Data were presented as a scatter dot plot with means (n = 4 for wild-type control, n = 5 for G14098A F1 rats). Significance was calculated with unpaired two-tailed Student’s t-test (*P < 0.05, **P < 0.01, ***P < 0.001).

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