Figure 1.

bax acts in a p53 pathway for drug-induced apoptosis. (A) Retroviruses expressing an E1A 12S cDNA and puro (LPC-12S; closed symbols) or a puro alone (LPC; open symbols) were used to infect MEFs derived from wild-type (circles), bax^−/− (triangles), and p53^−/− (squares) mice. Pure populations of E1A-expressing cells or controls were plated in multiwell plates and treated with the chemotherapeutic drug adriamycin. Cell viability was assessed 24 h later by trypan blue exclusion. The wild-type and bax^−/− MEFs were from littermate embryos. Each experiment used two separate MEF preparations for each genotype, and the data were pooled. Each point represents the mean ± SD from at least three separate experiments (n ≥ 6 for each genotype). (B) Wild type (white), bax^−/− (gray), and p53^−/− (black) MEFs expressing E1A were treated with etoposide (2 μg/ml) or pulsed for 1 h with cis-platinum (100 μM), and viability was assessed after 24 h. (C) The normal and E1A-expressing cell populations described in A, together with bax^+/−p53^−/− (closed diamond) and bax^−/−p53^−/− (open diamond) E1A-MEFs, were treated with high doses of adriamycin to induce p53-independent apoptosis. Viability was assessed 24 h later. Each experiment used two separate MEF preparations for each genotype; the p53^+/−bax^−/− and p53^−/−bax^−/− E1A-MEFs were derived from littermate embryos.