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.
journal_name
Celljournal_title
Cellauthors
Brodsky MH,Nordstrom W,Tsang G,Kwan E,Rubin GM,Abrams JMdoi
10.1016/S0092-8674(00)80627-3subject
Has Abstractpub_date
2000-03-31 00:00:00pages
103-13issue
1eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80627-3journal_volume
101pub_type
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