FIGURE 6.
DNA damage itself, not DNA damage repair pathways, is responsible for PNC disassembly. A, immunofluorescent staining to PTB to show PNCs in HeLa cells prior to UV treatment, 5 h post-100 mJ/m2 UV light, and 24 h post 100 mJ/m2 UV light. B, ATM/ATR activity was inhibited in HeLa cells with the small molecule inhibitor CGK-733. Cells were pretreated with 2 μm CGK-733 or vehicle for 4 h, then dosed with 100 mJ/m2 UV light, and returned to CGK-733 or vehicle, and then PNC prevalence was determined 5 and 24 h after UV light treatment. C, HeLa cells were pretreated with 2 μm CGK-733 or vehicle for 4 h, then treated with the [GI99%] (2.01 μm) of mitoxantrone in the presence of 2 μm CGK-733 or vehicle, and then PNC prevalence was determined 20 h after mitoxantrone treatment. Mitoxantrone was then removed, and cells were grown in the presence of 2 μm CGK-733 or vehicle for 24 or 48 h to allow PNC reformation, and the PNC was prevalence was determined (n = 3, error bars =±S.D.).