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. 2019 Dec 20;5(12):eaay2118. doi: 10.1126/sciadv.aay2118

Fig. 1. Heart and skeletal muscle conditional knockout of mouse Mtif3 causes cardiomyopathy.

Fig. 1

(A) Schematic showing the homologous recombination at the Mtif3 locus to generate conditional knockout mice. LoxP sites were introduced to allow the deletion of exon 3 by Cre recombinase. (B) Development of embryos of Mtif3+/+ and constitutive Mtif3−/− mice at embryonic day 8.5 (E8.5). (C) Weight differences between control (L/L) and knockout (L/L, cre) mice from 3 to 25 weeks of age. (D) Heart weight–to–tibia length ratio in control (L/L) and knockout (L/L, cre) mice at 10 and 25 weeks. (E) Echocardiographic parameters for control (L/L), and knockout (L/L, cre), 10- and 25-week-old mice. LVIDd, left ventricular end diastolic diameter; LVIDs, left ventricular end systolic diameter; FS, fractional shortening; LVPWd, left ventricular posterior wall in diastole; LVPWs, left ventricular posterior wall in systole; IVSd, intraventricular septum in diastole; IVSs, intraventricular septum in systole; HR, heart rate. (F) Heart and skeletal muscle sections cut to 5-μm thickness from 10-week-old and (G) 25-week-old L/L and L/L, cre mice were stained with H&E; yellow arrows show centralized nuclei in the skeletal muscle. Scale bars, 100 μm. All values are means ± SEM of n = 5. *P < 0.05, **P < 0.01, ***P < 0.001, Student’s t test.