Format

Send to

Choose Destination
Cell Death Differ. 2014 Mar;21(3):407-15. doi: 10.1038/cdd.2013.154. Epub 2013 Oct 25.

Bendless modulates JNK-mediated cell death and migration in Drosophila.

Author information

1
Department of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China.
2
1] Department of Interventional Radiology, Shanghai 10th People's Hospital, Shanghai Key Laboratory of Signaling and Disease Research, School of Life Science and Technology, Tongji University, Shanghai, China [2] Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, New Haven, CT 06519, USA.
3
1] Howard Hughes Medical Institute, Department of Genetics, Yale University School of Medicine, New Haven, CT 06519, USA [2] Institute of Developmental Biology and Molecular Medicine, Fudan-Yale Center for Biomedical Research, School of Life Sciences, Fudan University, Shanghai, China.

Abstract

The TNF-JNK pathway is a highly conserved signaling pathway that regulates a wide spectrum of biological processes including cell death and migration. To further delineate this pathway, we carried out a genetic screen for dominant modifiers of the cell death phenotype triggered by ectopic expression of Eiger (Egr), the Drosophila TNF ortholog. Here we show that Bendless (Ben), an E2 ubiquitin-conjugating enzyme, modulates Egr-induced JNK activation and cell death through dTRAF2. Furthermore, Ben physically interacts with dTRAF2 and regulates Egr-induced dTRAF2 polyubiquitination. Finally, Ben is required for JNK-dependent tumor progression, cell migration, oxidative stress resistance and longevity. Our results indicate that Ben constitutes an essential component of the evolutionarily conserved TNF-JNK pathway that modulates cell death and invasion, tumor progression, stress response and lifespan in metazoans.

PMID:
24162658
PMCID:
PMC3921588
DOI:
10.1038/cdd.2013.154
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center