Fig. 4: Loss of SDHAF4 disrupts complex II assembly and promotes mitochondrial dysfunction.

a Immunoblots for SDHAF4 and complex II subunits in left ventricles of WT mice at different ages. b, c Immunoblots for SDHAF4 and mitochondrial complex subunits in left ventricles of hearts from WT and Sdhaf4 mutant mice at age of 3 weeks (b, representative blotting image; c, summary analysis of arbitrary unit, n = 6, P < 0.0001). d mRNA levels of Sdha, Sdhb, Sdhc, and Sdhd in left ventricles of hearts from WT and Sdhaf4 mutant mice (n = 6). e Coimmunoprecipitation of SDHB, SDHC, and SDHD with SDHA from the lysates of left ventricles of hearts from WT and Sdhaf4 mutant mice at age of 3 weeks. f Coimmunoprecipitation of SDHA, SDHC, and SDHD with SDHB from the lysates of left ventricles of hearts from WT and Sdhaf4 mutant mice at age of 3 weeks. g Coimmunoprecipitation of SDHA, SDHB, SDHC, and SDHD with Ubiquitin from the lysates of left ventricles of hearts from WT and Sdhaf4 mutant mice at age of 3 weeks. h Immunoblots for mitochondrial supercomplex: mitochondrial proteins of left ventricles of hearts from WT and Sdhaf4 mutant mice were subjected to BN-PAGE and immunoblot with NDUFA9 (subunit of Complex I), UQCRC1 (subunit of Complex III), and COX4 (subunit of complex IV) antibodies. i, Analysis of complex activities of mitochondrion from left ventricles of hearts from WT and Sdhaf4 mutant mice at age of 3 weeks, n = 6, P = 0.0002. j–k Mitochondrial oxygen consumption rate (OCR, P = 0.013, 0.026, 0.015, 0.003, 0.001, 0.00013) and ATP level of left ventricles of hearts (P = 0.002) from WT and Sdhaf4 mutant mice at age of 3 and 8 weeks, n = 9. Values are mean ± SEM, *P < 0.05, **P < 0.01. Statistical significance was determined by two-tailed Student’s t-test (c, d, i–k). Source data are provided in Source Data file.