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Autophagy as a trigger for cell death : autophagic degradation of inhibitor of apoptosis dBruce controls DNA fragmentation during late oogenesis in Drosophila
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Nezis, I. P., Shravage, Bhupendra V., Sagona, Antonia P., Johansen, Terje, Baehrecke, Eric H. and Stenmark, H. (Harald) (2010) Autophagy as a trigger for cell death : autophagic degradation of inhibitor of apoptosis dBruce controls DNA fragmentation during late oogenesis in Drosophila. Autophagy, Vol. 6 (No. 8). pp. 1214-1215. doi:10.4161/auto.6.8.13694
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Official URL: http://dx.doi.org/10.4161/auto.6.8.13694
Abstract
Autophagy has been reported to contribute to cell death, but the underlying mechanisms remain largely unknown and controversial. We have
been studying oogenesis in Drosophila melanogaster as a model system to understand the interplay between autophagy and cell death. Using a novel autophagy reporter we found that autophagy occurs during developmental cell death of nurse cells in late oogenesis. Genetic inhibition
of autophagy-related genes atg1, atg13 and vps34 results in late-stage egg chambers containing persisting nurse cell nuclei without fragmented DNA and attenuation of caspase-3 cleavage. We found that Drosophila inhibitor of apoptosis dBruce is degraded by autophagy and this degradation promotes DNA fragmentation and subsequent nurse cell death. These studies demonstrate that autophagic degradation of an inhibitor
of apoptosis is a novel mechanism of triggering cell death
| Item Type: | Journal Article | ||||
|---|---|---|---|---|---|
| Divisions: | Faculty of Science, Engineering and Medicine > Science > Life Sciences (2010- ) | ||||
| Journal or Publication Title: | Autophagy | ||||
| Publisher: | Landes Bioscience | ||||
| ISSN: | 1554-8627 | ||||
| Official Date: | 2010 | ||||
| Dates: |
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| Volume: | Vol. 6 | ||||
| Number: | No. 8 | ||||
| Page Range: | pp. 1214-1215 | ||||
| DOI: | 10.4161/auto.6.8.13694 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access |
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