The tumor suppressor protein p53 functions as a checkpoint in the G1 phase of the cell cycle, responding to DNA damage. Mutations in the p53 gene lead to genomic instability and tumor formation. The E2F-1 transcription factor, which is a partner of the retinoblastoma-susceptibility gene product (RB), regulates entry into the S phase. To explore the interaction between p53 and E2F-1, a human E2F-1 expression plasmid was introduced into a murine cell line containing a temperature-sensitive p53 allele. Coexpression of wild-type p53 and E2F-1 resulted in rapid cell death through apoptosis. This suggests that the cell cycle utilizes an interacting pathway between RB-E2F-1 and p53. The study also found that E2F-1 overcame the p53-mediated growth arrest, leading to cell death. The results provide insights into the communication between tumor suppressor genes RB and p53 in checkpoint control of the cell cycle.The tumor suppressor protein p53 functions as a checkpoint in the G1 phase of the cell cycle, responding to DNA damage. Mutations in the p53 gene lead to genomic instability and tumor formation. The E2F-1 transcription factor, which is a partner of the retinoblastoma-susceptibility gene product (RB), regulates entry into the S phase. To explore the interaction between p53 and E2F-1, a human E2F-1 expression plasmid was introduced into a murine cell line containing a temperature-sensitive p53 allele. Coexpression of wild-type p53 and E2F-1 resulted in rapid cell death through apoptosis. This suggests that the cell cycle utilizes an interacting pathway between RB-E2F-1 and p53. The study also found that E2F-1 overcame the p53-mediated growth arrest, leading to cell death. The results provide insights into the communication between tumor suppressor genes RB and p53 in checkpoint control of the cell cycle.