Eiger, the sole Drosophila TNF-alpha homolog, causes ectopic apoptosis through JNK pathway activation. Yet, its role in developmental apoptosis remains unclear. eiger mutant flies are viable and fertile but display compromised elimination of oncogenic cells and extracellular bacteria. Here we show that Eiger, specifically expressed in embryonic neurons and glia, is not involved in developmental neuronal apoptosis or in apoptotic cell clearance. Instead, we provide evidence that Eiger is required for damage-induced apoptosis in the embryonic CNS through regulation of the pro-apoptotic gene hid independently of the JNK pathway. Our study thus reveals a new requirement for Eiger in eliminating damaged cells during development.
Bibliographical noteFunding Information:
We would like to thank B. Jones, D. Bohmann, G.W. Davis, E. Arama, H. Steller, M. Miura, O. Schuldiner, A. Salzberg, Hybridoma bank and the Bloomington Stock Center for generously providing fly strains and antibodies. We thank Dr. Alexander Nevelsky and Egor Borzov from Department of Oncology, Rambam Medical Center (RMC) for their assistance in the X-ray experiments. We thank Z. Paroush and T. Schultheiss for comments on the manuscript and the Kurant laboratory members for constructive criticism and support. We also thank E. Suss-Toby at the Interdepartmental Bioimaging facility for excellent technical support. We gratefully acknowledge financial support from Rappaport Institute and from Allen and Jewell Prince Center for Neurodegenerative Disorders of the Brain.
© 2015 The Authors. Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies. This is an open access article under the CC BY-NC-ND license.
ASJC Scopus subject areas
- Structural Biology
- Molecular Biology
- Cell Biology