Extended Data Fig. 5: Phenotypic consequences of altered TMEM65 expression.
From: TMEM65 regulates and is required for NCLX-dependent mitochondrial calcium efflux
a, Representative images showing WGA labelling (green) and nuclear staining with DAPI (blue) in cross sections of the gastrocnemius muscle at 24 weeks of age. scr., scrambled. b, Total mass of the gastrocnemius + soleus + plantaris muscle, dissected as a unit, normalized to total body mass at 24 weeks of age. Open symbols represent male mice, filled symbols represent female mice throughout. (n = 10 mice + scrambled shRNA, 9 mice + Tmem65 shRNA. P-value by unpaired two-tailed t-test with Welch’s correction). Left ventricular end diastolic dimension (LVEDD) (c) and left ventricular end systolic dimension (LVESD) (d) as measured by echocardiography in mice at 6 weeks of age (n = 11 mice + scrambled shRNA, 7 mice + Tmem65 shRNA. P-values by unpaired two-tailed t-test). e, Pooled traces showing extramitochondrial bath Ca2+ (Fura-FF) and mitochondrial membrane potential (JC-1) in permeabilized WT and TMEM65−/− AC16 cardiomyocytes in response to repeated additions of 5 µM Ca2+ (arrows). Red arrows indicate the Ca2+ bolus typically triggering permeability transition in each genotype. (n = 3 replicates/genotype). f, Pooled traces showing extramitochondrial bath Ca2+ (Fura-FF) and mitochondrial membrane potential (JC-1) in permeabilized control or TMEM65-OE AC16 cardiomyocytes in response to repeated additions of 10 µM Ca2+ (arrows). Red arrow indicates Ca2+ bolus triggering permeability transition in control cells. (n = 4 replicates for empty vector controls, 5 replicates for TMEM65-OE). Data are presented as mean ± SEM.
