Journal
DEVELOPMENTAL BIOLOGY
Volume 346, Issue 1, Pages 80-89Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2010.07.023
Keywords
Drosophila; Radiation; Apoptosis; p53; E2F
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Funding
- NIGMS NIH HHS [R01 GM66441, R01 GM87276, R01 GM066441, R01 GM087276] Funding Source: Medline
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The ability of ionizing radiation (IR) to induce apoptosis independent of p53 is crucial for successful therapy of cancers bearing p53 mutations. p53-independent apoptosis, however, remains poorly understood relative to p53-dependent apoptosis. IR induces both p53-dependent and p53-independent apoptoses in Drosophila melanogaster, making studies of both modes of cell death possible in a genetically tractable model. Previous studies have found that Drosophila E2F proteins are generally pro-death or neutral with regard to p53-dependent apoptosis. We report here that dE2F1 promotes IR-induced p53-independent apoptosis in larval imaginal discs. Using transcriptional reporters, we provide evidence that, when p53 is mutated, dE2F1 becomes necessary for the transcriptional induction of the pro-apoptotic gene hid after irradiation. In contrast, the second E2F homolog, dE2F2, as well as the net E2F activity, which can be depleted by mutating the common cofactor, dDp, is inhibitory for p53-independent apoptosis. We conclude that p53-dependent and p53-independent apoptoses show differential reliance on E2F activity in Drosophila. (C) 2010 Elsevier Inc. All rights reserved.
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