Extended Data Fig. 6: TrnE mutation in the liver doesn’t cause detectable defects.
a, Liver morphology from 100-week-old mice with low and high TrnE mutation. The annotated mutation load represents the tail’s mutation at the time of dissection. Scale bar = 1 cm. b, First row: HE staining of paraformaldehyde-fixed, paraffin-embedded liver sections (5 μm thickness) from 100-week-old WT and TrnE mice. Second row: Oil-red O staining of liver frozen sections from 100-week-old WT and TrnE mice. (section thickness = 10 μm). Third row: NBTx staining of liver frozen sections from 100-week-old WT and TrnE mice (section thickness = 10 μm). Fourth row: TEM images of hepatocyte mitochondria from 100-week-old WT and TrnE high-mutant mice livers. Fifth row: high magnification view of mitochondria from the fourth row. c, Western blot of 100-week-old control (0–4%) and TrnE high-mutant group (75–81%) livers for OXPHOS complex subunits. TOM20 and ACTB shown as the loading control. d, Quantification of OXPHOS complex subunits in c (mean ± SD, n = 4. Unpaired two-tailed Student’s t-test). e, Plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), cholesterol (CHOL), and triglyceride (TG) (mean ± SD, n = 5–7 per group. Unpaired two-tailed Student’s t-test) in 100-week-old mice. f, mtDNA copy number quantification in bulk liver from control and TrnE high-mutant mice at 3 and 75 weeks of age (mean ± SEM, n = 3–4 per group. Unpaired two-tailed Student’s t-test).
