Fig. 4. TRF2^ΔBΔM-induced growth arrest in murine cells depends on p53. (A) S-phase index of TRF2^ΔBΔM-expressing p53^+/+ and p53^–/– MEFs. Cells of the indicated genotypes were infected with the TRF2^ΔBΔM virus or the vector control, and the incorporation of BrdU in the parallel cultures was measured as described in Figure 2B. The bar graph shows the percentage of TRF2^ΔBΔM-expressing cells in S phase compared with controls (control virus infection set at 100%) as measured using BrdU incorporation. Two experiments are shown for two independent batches of MEFs deficient in p53. (B) Effects of deficiency for p53, p21, p19^Arf or p16 on the TRF2^ΔBΔM-induced growth arrest in MEFs. Cells of the indicated genotypes were infected with TRF2^ΔBΔM or a control virus. BrdU incorporation in TRF2^ΔBΔM-expressing cells was normalized to control infected cells as described in Figure 2B. Values are derived from triplicate measurements. SDs were 1–5%. (C) Effects of p53, p21, p19^Arf and p16 status on the TRF2^ΔBΔM-induced morphology and SA-β-gal expression. Cells used in the experiment shown in (B) were plated at equal cell density on day 10 and assayed for β-gal activity 2 days later. (D) Levels of p21 and p16 in mouse cells expressing TRF2^ΔBΔM. Cells of the indicated genotypes were infected with the TRF2^ΔBΔM virus or the vector control. Lysates (10⁴ cells/lane) were prepared on day 10.