Fig. 4.

A second DNA damage signal input to Bcl-2. (A) Degradation of Bcl-2 protein in p53^−/−;E2f1^−/− is prevented by repairing cyclobutane pyrimidine dimers after UVB. Cells were pretreated for 1 h with 150 μl of photolyase in liposomes or empty liposomes. Both sets were irradiated with 750 J/m² UVB and illuminated with UVA for 5 min to activate the photolyase- and monomerize-bound cyclobutane pyrimidine dimers in DNA, and blots were analyzed for Bcl-2 protein. Each point represents an average of three independent experiments on cells from seven mice. The two treatments are statistically different at 1, 3, 9, and 12 h (P = 0.04, 0.04, 0.04, and 0.02, respectively). (B) Photolyase suppresses UVB-induced apoptosis in p53^−/−;E2f1^−/− fibroblasts. Cells were treated with photolyase, UVB, and UVA as before and incubated for 20 h, and apoptosis was measured. Each bar represents an average of three repeats with cells from 10 mice. The samples are statistically different (∗, P = 0.04).