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. 2020 Jul 14;295(35):12485–12497. doi: 10.1074/jbc.RA119.011229

Figure 1.

Figure 1.

Taz deficiency disrupts mitochondrial membrane composition and supercomplex integrity but not cardiac function. A, graphical summary (n = 6/group) and representative immunoblot of ∼30-kDa tafazzin protein detected in cardiac mitochondria from WT mice, but not Taz shRNA (TazKD) mice. B and C, fatty acid composition of cardiolipin (B) and total phospholipids (PL, C) extracted from SS and IF cardiac mitochondria (n = 4–6/group). D, representative images of high-molecular-mass protein complexes separated from WT and TazKD cardiac mitochondria by blue native (BN)–PAGE, subsequently probed for respiratory chain complexes I–V by SDS-PAGE (full analysis in Fig. S2). E, echocardiographic measures of left ventricular end-diastolic dimensions (EDD) and end-systolic dimensions (ESD) and corresponding fractional shortening (FS; [(EDD − ESD)/EDD × 100]) for 4–6-month-old WT and TazKD mice (n = 12/group). *, P < 0.01 for WT versus TazKD.