Screening of suppressors of bax-induced cell death identifies glycerophosphate oxidase-1 as a mediator of debcl-induced apoptosis in Drosophila
Jessie Colin1,2,*, Julie Garibal1,2,*, Amandine Clavier1,2, Sébastien Szuplewski1, Yanick Risler1, Cécile Milet1,2, Sébastien Gaumer1, Isabelle Guénal1,3 and Bernard Mignotte1,2,3
1 Université Versailles St-Quentin, EA4589, Laboratoire de Génétique et Biologie Cellulaire, 78180 Montigny-le-Bretonneux, France.
2 Ecole Pratique des Hautes Etudes, Laboratoire de Génétique Moléculaire et Physiologique, 78180 Montigny-le-Bretonneux, France
3 Co-senior authors
* These two authors contributed equally to this work
Correspondence:
Bernard Mignotte, email:
Keywords: Apoptosis, Bax, Debcl, mutagenesis, Glycerophosphate oxidase
Received: February 9, 2015 Accepted: June 6, 2015 Published: June 10, 2015
Abstract
Members of the Bcl-2 family are key elements of the apoptotic machinery. In mammals, this multigenic family contains about twenty members, which either promote or inhibit apoptosis. We have previously shown that the mammalian pro-apoptotic Bcl-2 family member Bax is very efficient in inducing apoptosis in Drosophila, allowing the study of bax-induced cell death in a genetic animal model. We report here the results of the screening of a P[UAS]-element insertion library performed to identify gene products that modify the phenotypes induced by the expression of bax in Drosophila melanogaster. We isolated 17 putative modifiers involved in various function or process: the ubiquitin/proteasome pathway; cell growth, proliferation and death; pathfinding and cell adhesion; secretion and extracellular signaling; metabolism and oxidative stress. Most of these suppressors also inhibit debcl-induced phenotypes, suggesting that the activities of both proteins can be modulated in part by common signaling or metabolic pathways. Among these suppressors, Glycerophosphate oxidase-1 is found to participate in debcl-induced apoptosis by increasing mitochondrial reactive oxygen species accumulation.
