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. 2016 Feb 4;35(7):724–742. doi: 10.15252/embj.201592862

Figure 3. PGC‐1β‐dependent mitochondrial biogenesis downstream of the DDR modulates cellular senescence.

Figure 3

  1. Representative images of colony assays of wild‐type and PGC‐1β −/− MEFs grown at 3 or 21% O2 (10 days after seeding 5,000 cells per well). Data are representative of 3 independent experiments.
  2. Effect of 3 or 21% O2 and X‐ray irradiation (at 3% O2) on the percentage of Ki67 (at day 6) and Sen‐β‐Gal‐positive cells (at day 10) and the number (N) of 53BP1 foci (at day 6) in wild‐type and PGC‐1β −/− MEFs. Data are mean ± SEM of n = 3 independent experiments; asterisks denote a statistical significance at P < 0.05 using one‐way ANOVA.
  3. Representative images of Sen‐β‐Gal activity (blue cytoplasmatic staining), Ki‐67 and 53BP1 foci in proliferating and senescent wild‐type and PGC‐1β −/− MEFs (scale bar = 10 μm).
  4. mRNA expression of PGC‐1β,CXCL‐1 and p16 in proliferating and senescent (10 days after 10‐Gy X‐ray) wild‐type and PGC‐1β −/− MEFs. Data are mean ± SEM of n = 3 independent experiments; asterisks denote a statistical significance at P < 0.05 using one‐way ANOVA.
  5. Effects of overexpression of PGC‐1β on percentage of Ki67‐ and Sen‐β‐Gal‐positive cells, number (N) of 53BP1 foci and percentage change in mitochondrial mass (NAO intensity) in proliferating and senescent (2 days after 10‐Gy X‐ray) MEFs cultured at 3% O2. Data are mean ± SEM of n = 3 independent experiments. Asterisks denote a statistical significance at P < 0.05 using one‐way ANOVA or two‐tailed t‐test.