Drosophila p53 binds a damage response element at the reaper locus

Michael H. Brodsky, William Nordstrom, Garson Tsang, Elaine Kwan, Gerald M. Rubin, John M. Abrams

Research output: Contribution to journalArticlepeer-review

366 Scopus citations

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 languageEnglish (US)
Pages (from-to)103-113
Number of pages11
JournalCell
Volume101
Issue number1
DOIs
StatePublished - Mar 31 2000

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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