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. 2014 Dec;24:122–130. doi: 10.1016/j.dnarep.2014.09.001

Fig. 5.

Fig. 5

Proper cell cycle progression and chromosomal segregation depends on ATMIN following aphidicolin treatment. (A) ATMIN+/+ and ATMINΔ/Δ MEFs were treated with 1 μM aphidicolin for 24 h followed by analysis by immunoblotting with the indicated antibodies. For FANCD2 ‘Ratio’ denotes the amount of monoubiquitinated (Mono-Ub) compared to unmodified FANCD2. ‘Fold induction’ denotes the increase in monoubiquitinated FANCD2 in aphidicolin treated samples as compared with the corresponding control treated sample. (B) ATMIN+/+ and ATMINΔ/Δ MEFs were either treated with DMSO, 1 μM aphidicolin (Aph.) for 24 h or 1 μM aphidicolin (Aph.) for 24 h followed by incubation in drug-free media for 8 h (8 h release) and cell cycle profiles were analyzed by propidium iodide staining. C. ATMIN+/+ and ATMINΔ/Δ MEFs were treated with 1 μM aphidicolin for 24 h followed by incubation in drug-free media for 8 h and stained with DAPI. Defects in cell division marked by lagging chromosomes and anaphase bridges were imaged and quantified as were cells displaying formation of micronuclei (D). At least 200 cells were analyzed per condition. **p < 0.01, ***p < 0.001.