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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: DNA Repair (Amst). 2014 May 10;21:131–139. doi: 10.1016/j.dnarep.2014.04.008

Figure 5.

Figure 5

DNA-PKcs – RPA32 signaling suppresses mitotic catastrophe after replication stress. (A) Representative images of WT, DNA-PKcs null and KD cells after 16 h treatment with 10 mM HU and staining with DAPI (blue) and anti-tubulin antibodies (green). A higher HU concentration was used in this experiment to increase sensitivity to detect abnormal cells. Arrows indicate anaphase bridges (failed cytokinesis) and giant cells. (B) Average percentage (±SEM) of abnormal cells for 4 determinations. (C) Images of mitotic RPA32 S4A/S8A and WT cells stained with DAPI following etoposide or mock treatment. WT cells treated with etoposide are not shown because they arrest before M phase. In etoposide-treated cells, arrows indicate anaphase bridges (left and center) and nuclear blebs (left and right).