Volume 22, No 2, Feb 2012

ISSN: 1001-0602 
EISSN: 1748-7838 2018 
impact factor 17.848* 
(Clarivate Analytics, 2019)

Volume 22 Issue 2, February 2012: 425-431

ORIGINAL ARTICLES

NOPO modulates Egr-induced JNK-independent cell death in Drosophila

Xianjue Ma, Jiuhong Huang, Lixia Yang, Yang Yang, Wenzhe Li and Lei Xue

Shanghai Key Laboratory for Signaling and Diseases, School of Life Science and Technology, Tongji University, 1239 Siping Road, Shanghai 200092, China Correspondence: Lei Xue,(lei.xue@tongji.edu.cn)

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.

Cell Research (2012) 22:425-431. doi:10.1038/cr.2011.135; published online 16 August 2011

FULL TEXT | PDF

Browse 1958