Abstract
The tumor suppressor genep53 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.
Original language | English (US) |
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Pages (from-to) | 103-113 |
Number of pages | 11 |
Journal | Cell |
Volume | 101 |
Issue number | 1 |
DOIs | |
State | Published - Mar 31 2000 |
ASJC Scopus subject areas
- General Biochemistry, Genetics and Molecular Biology