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. 2014 Jan 6;23(10):2580–2592. doi: 10.1093/hmg/ddt652

Figure 1.

Figure 1.

Loss of LRPPRC results in OXPHOS dysfunction. (A) The COX enzyme activity was measured in heart mitochondria from Lrpprc knockout and control at age 4 weeks (4w), 8 weeks (8w) and 12 weeks (12w). Open bars, controls (n = 4); filled bars, knockouts (n = 4). Error bars indicate mean ± SEM (*P < 0.05; **P < 0.01; ***P < 0.001). (B) Oxygen consumption of heart mitochondria from Lrpprc knockout and control at different ages. Isolated mitochondria were incubated with substrates feeding electrons to complex I (pyruvate, glutamate, malate) or complex II (succinate combined with complex I inhibition by rotenone). Each set of substrates was successively combined with ADP (to assess the phosphorylating respiration: state 3), oligomycin (to measure the non-phosphorylating respiration: state 4) and finally uncoupled by adding an increasing concentration of CCCP. Open bars, control [n = 4 (at age 4 and 8 weeks) n = 15 (at age 12 weeks)]; filled bars, knockout [n = 4 (at age 4 and 8 weeks) n = 15 (at age 12 weeks)]. Error bars indicate means ± SEM (*P < 0.05; **P < 0.01; ***P < 0.001). (C) ATP synthesis flux assessed in heart mitochondria from Lrpprc knockout and control at the age of 12 weeks, in the presence of succinate and rotenone. Open bars, control (n = 3–4); filled bars, knockout (n = 3–4). Error bars indicate means ± SEM (*P < 0.05; **P < 0.01; ***P < 0.001). (D) Measurement of the oxidative phosphorylation coupling yield (nmol ATP/natO) in heart mitochondria from Lrpprc knockout and controls at different ages. Open bars, control (n = 4); filled bars, knockout (n = 4). Error bars indicate means ± SEM (*P < 0.05; **P < 0.01; ***P < 0.001).