The Drosophila caspase DRONC is regulated by DIAP1

The Drosophila caspase DRONC is regulated by DIAP1 We have isolated the recently identified Drosophila caspase DRONC through its interaction with the effector caspase drICE. Ectopic expression of DRONC induces cell death in Schizosaccharomyces pombe, mammalian fibroblasts and the developing Drosophila eye. The caspase inhibitor p35 fails to rescue DRONC‐induced cell death in vivo and is not cleaved by DRONC in vitro, making DRONC the first identified p35‐resistant caspase. The DRONC pro‐domain interacts with Drosphila inhibitor of apoptosis protein 1 (DIAP1), and co‐expression of DIAP1 in the developing Drosophila eye completely reverts the eye ablation phenotype induced by pro‐DRONC expression. In contrast, DIAP1 fails to rescue eye ablation induced by DRONC lacking the pro‐domain, indicating that interaction of DIAP1 with the pro‐domain of DRONC is required for suppression of DRONC‐mediated cell death. Heterozygosity at the diap1 locus enhances the pro‐DRONC eye phenotype, consistent with a role for endogenous DIAP1 in suppression of DRONC activation. Both heterozygosity at the dronc locus and expression of dominant‐negative DRONC mutants suppress the eye phenotype caused by reaper (RPR) and head involution defective (HID), consistent with the idea that DRONC functions in the RPR and HID pathway. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The EMBO Journal Wiley

The Drosophila caspase DRONC is regulated by DIAP1

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Publisher
Wiley
Copyright
Copyright © 2013 Wiley Periodicals, Inc
ISSN
0261-4189
eISSN
1460-2075
D.O.I.
10.1093/emboj/19.4.598
Publisher site
See Article on Publisher Site

Abstract

We have isolated the recently identified Drosophila caspase DRONC through its interaction with the effector caspase drICE. Ectopic expression of DRONC induces cell death in Schizosaccharomyces pombe, mammalian fibroblasts and the developing Drosophila eye. The caspase inhibitor p35 fails to rescue DRONC‐induced cell death in vivo and is not cleaved by DRONC in vitro, making DRONC the first identified p35‐resistant caspase. The DRONC pro‐domain interacts with Drosphila inhibitor of apoptosis protein 1 (DIAP1), and co‐expression of DIAP1 in the developing Drosophila eye completely reverts the eye ablation phenotype induced by pro‐DRONC expression. In contrast, DIAP1 fails to rescue eye ablation induced by DRONC lacking the pro‐domain, indicating that interaction of DIAP1 with the pro‐domain of DRONC is required for suppression of DRONC‐mediated cell death. Heterozygosity at the diap1 locus enhances the pro‐DRONC eye phenotype, consistent with a role for endogenous DIAP1 in suppression of DRONC activation. Both heterozygosity at the dronc locus and expression of dominant‐negative DRONC mutants suppress the eye phenotype caused by reaper (RPR) and head involution defective (HID), consistent with the idea that DRONC functions in the RPR and HID pathway.

Journal

The EMBO JournalWiley

Published: Feb 15, 2000

References

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