Fig. 2: Ablation of MRM2 leads to a severe impairment of cellular respiration and dysfunction of MRC complexes.
From: A late-stage assembly checkpoint of the human mitochondrial ribosome large subunit

a Cell proliferation in glucose (Glc) or galactose (Gal) media. Data are presented as mean ± SD (n = 8, independent measurements). b Oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) measurements in the presence of mitochondrial respiration inhibitors (O: oligomycin; B: BAM15; R + A: rotenone and antimycin A). Data are presented as mean ± SD (n = 22 for parental, n = 23 for MRM2 knock-out, independent measurements). c Spectrophotometric determination of the activity of MRC complexes (CI: complex I, NADH:ubiquinone oxidoreductase; CII: complex II, succinate:ubiquinone oxidoreductase; CIII: complex III, ubiquinol:cytochrome c oxidoreductase; CIV: complex IV, cytochrome c oxidase). n.d.: no data. Experimental values and mean ± SD are shown. Statistical significance was assessed using two-tailed Student’s t test (∗∗: P ≤ 0.01; ∗∗∗: P ≤ 0.001; CI Parental vs MRM2 KO P = 0.0023, CIII Parental vs MRM2 KO P = 0.0001). Data from parental and MRM2 knock-out (KO) cell lines are represented in black and red, respectively. Source data are provided as a Source Data file.