Journal
CELL RESEARCH
Volume 22, Issue 2, Pages 425-431Publisher
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2011.135
Keywords
cTNF; JNK; NOPO; caspase; cell death
Categories
Funding
- National Natural Science Foundation of China [30971681, 31071294]
- National Basic Research Program of China (973 Program) [2010CB944901, 2011CB943903]
- Shanghai Pujiang Program [09PJ1409400]
- Shanghai Municipal Education Commission [10ZZ27]
- Program for New Century Excellent Talents in University [NCET-10-0608]
- Shanghai Committee of Science and Technology [09DZ2260100]
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Tumor necrosis factor (TNF) family ligands play essential roles in regulating a variety of cellular processes including proliferation, differentiation and survival. Expression of Drosophila TNF ortholog Eiger (Egr) induces JNK-dependent cell death, while the roles of caspases in this process remain elusive. To further delineate the Egr-triggered cell death pathway, we performed a genetic screen to identify dominant modifiers of the Egr-induced cell death phenotype. Here we report that Egr elicits a caspase-mediated cell death pathway independent of JNK signaling. Furthermore, we show NOPO, the Drosophila ortholog of TRIP (TRAF interacting protein) encoding an E3 ubiquitin ligase, modulates Egr-induced Caspase-mediated cell death through transcriptional activation of pro-apoptotic genes reaper and hid. Finally, we found Bendless and dUEV1a, an ubiquitin-conjugating E2 enzyme complex, regulates NOPO-triggered cell death. Our results indicate that the Ben-dUEV1a complex constitutes a molecular switch that bifurcates the Egr-induced cell death signaling into two pathways mediated by JNK and caspases respectively.
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