Drosophila p53 Binds a Damage Response Element at the reaper Locus

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/S0092-8674(00)80627-3 Byline: Michael H Brodsky (1), William Nordstrom (2), Garson Tsang (1), Elaine Kwan (1), Gerald M Rubin (1), John M Abrams (2) Abstract: The tumor suppressor gene p53 regulates multiple cellular responses to DNA damage, but the transcriptional targets that specify these responses are incompletely understood. We describe a Drosophila p53 homolog and demonstrate that it can activate transcription from a promoter containing binding sites for human p53. Dominant-negative forms of Drosophila p53 inhibit both transactivation in cultured cells and radiation-induced apoptosis in developing tissues. The cis-regulatory region of the proapoptotic gene reaper contains a radiation-inducible enhancer that includes a consensus p53 binding site. 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 Drosophila p53 following DNA damage. Author Affiliation: (1) Howard Hughes Medical Institute, Department of Molecular and Cell Biology, University of California, Berkeley, California 94720, USA (2) Department of Cell Biology, University of Texas, Southwestern Medical Center, Dallas, Texas 75390, USA Article History: Received 3 March 2000; Revised 10 March 2000