Skip to main content
. Author manuscript; available in PMC: 2014 Jun 1.
Published in final edited form as: Aging Cell. 2013 Apr 24;12(3):467–477. doi: 10.1111/acel.12071

Figure 4.

Figure 4

Analysis of non-oxidative and oxidative DNA damage in liver and brain of mouse models of premature aging. QPCR efficacy of nuclear genome targets, with and without FPG treatment, was similar for DNA obtained from DNA-repair deficient mouse models of premature aging at terminal ages and DNA from young wild type animals (A). Although QPCR for the long mitochondrial genome target from the liver of Ku80 mutants was significantly less efficient than for DNA from either wild type or Ercc1−/Δ mutant animals (B), this difference is due to relative underrepresentation of mitochondrial DNA in the liver of Ku80 mutants, as demonstrated by real-time qPCR (C). QPCR assay was performed at least 3 times for each analyzed target; n=5 for each genotype. Data shown as average ±SD; asterisk (*) designates statistically significant difference with corresponding control (p<0.05).