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. Author manuscript; available in PMC: 2010 Jul 6.
Published in final edited form as: Cell Cycle. 2009 Sep 16;8(18):2951–2963. doi: 10.4161/cc.8.18.9539

Figure 5.

Figure 5

Long-term fate of post-mitotic, bleomycin treated cells. HCT116 cells were treated as described in legend of Figure 4. (A–D) show data of cells treated with bleomycin and UCN-01. (A) Post-mitotic, bleomycin treated cells either died after a prolonged interphase arrest (a), or alternatively, arrested in interphase (b). The time 0:00 corresponds to rounding up at mitosis onset. (B) 11% (n = 19) of bleomycin treated cells that did not go through mitosis died, but 72% (n = 37) of cells that progressed through mitosis died during the subsequent interphase. (C) Death in post-mitotic bleomycin treated cells (72%, n = 32) was only partly suppressed by poly-caspase inhibitor (40%, n = 38) or p53 knockout (29%, n = 42). The suppression observed under each of these conditions was similar to that observed in Z-VAD-FMK treated p53-/- cells (38%, n = 42), suggesting that p53 and caspase independent mechanisms contribute to cell death in the post-mitotic cells. (D) Fraction of parental and p53 mutant cells that initiated a second division following bleomycin treatment in the presence or absence of Z-VAD-FMK. Number of cells scored for each condition: 32 (a), 38 (b), 42 (c),42 (d). All p-values were based on a Z-score calculation.