Fig. 3: Tango2 deletion leads to cardiomyopathy and muscle weakness in vivo.

a Echocardiographic parameters for 20-week-old control and Tango2^–/– mice either fed NCD or HFD. LVIDd left ventricular internal diameter during diastole, LVIDs left ventricular internal diameter during systole, 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 (n = 5). All values are means ± SD, Student’s two-tailed t test. b Electron microscopy images of heart sections from 20-week-old control andTango2^–/– mice fed a NCD. The results are representative of at least three independent mice per genotype. c Hanging wire test in 20-week-old control and Tango2^–/– mice. Falling and reaching score was determined after 3 min (n = 7). d Involuntary treadmill exercise of 20-week-old control and Tango2^–/– mice (n = 7 per genotype). All values are means ± SD *p < 0.05, **p < 0.01 ***p < 0.001, ****p < 0.0001 Student’s two-tailed t test or Welch’s t test for (d). Proteomic changes in (e) heart and (f) skeletal muscle from 20-week-old Tango2^–/– mice fed a NCD compared to control mice (n = 5), and adjusted p values are shown in Supplementary Data 4. Significantly increased and decreased proteins were shown in red and blue, respectively, mitochondrial proteins are shown in green and Golgi proteins in purple. Gene ontology analyses show significantly changing reactome pathways in (g) heart and (h) skeletal muscle from 20-week-old Tango2^–/– mice fed a NCD compared to control mice (n = 5). The results show the top 20 pathways with the highest –log₁₀(FDR) and the colour scale represents fold change (FC) for each pathway and set size is the number of genes within each pathway.