Drosophila p53 binds a damage response element at the reaper locus

The tumor suppressor gene p53 regulates multiple cellular responses to DNA damage, but the transcriptional targets that specify these responses are in completely understood. We describe a Drosophila p53 homolog and demonstrate that it can activate transcription from a promoter containing binding site s for human p53. Dominant-negative forms of Drosophila p53 inhibit both tra nsactivation in cultured cells and radiation-induced apoptosis in developin g tissues. The cis-regulatory region of the proapoptotic gene reaper contai ns a radiation-inducible enhancer that includes a consensus p53 binding sit e. Drosophila p53 can activate transcription from this site in yeast and a multimer of this site is sufficient for radiation induction in vivo. These results indicate that reaper is a direct transcriptional target of Drosophi la p53 following DNA damage.