Enhanced oncogenic transformation in Chk1^Tg MEF. (A) Plates of WT and Chk1^Tg MEF 2 wk after infection with a Ras/E1A-expressing retrovirus. Colonies were stained with Methylene blue. Images are representative of six independent experiments. (B) Numbers of transformed colonies per plate in WT and Chk1^Tg MEF infected with Ras/E1A. Data derive from three independent experiments. (C) HTM-mediated quantification of γH2AX in WT and Chk1^Tg MEF 24 and 48 h after infection with a Ras/E1A-expressing retrovirus. Data are representative of three independent experiments. (D) Percentage of apoptotic cells present in cultures of WT and Chk1^Tg MEF 24 and 48 h after infection with a Ras/E1A-expressing retrovirus. The quantification derives from three independent experiments. (E) HTM-mediated quantification of γH2AX in WT and Chk1^Tg MEF infected with MycER, treated or untreated with 4-OHT for 8 or 24 h. Data are representative of three independent experiments. (F) MycER-induced apoptosis in WT and Chk1^Tg MEF infected with MycER, treated or untreated with 4-OHT for 72 h. Data derive from three independent experiments. (G) HTM-mediated analysis of γH2AX in WT and Chk1^Tg MEF infected with MycER and treated with 4-OHT for 24 h, which were previously infected with lentiviruses expressing a p53-specific shRNA (sh p53) or a control shRNA (sh C). Data are representative of three independent experiments. In B, D, and F, error bars indicate SD; in C–G, center lines indicate mean values. *, P < 0.05; **, P < 0.01; ***, P < 0.001.