Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/56687
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Type: Journal article
Title: Autophagy, not apoptosis, is essential for midgut cell death in Drosophila
Author: Denton, D.
Shravage, B.
Simin, R.
Mills, K.
Berry, D.
Baehrecke, E.
Kumar, S.
Citation: Current Biology, 2009; 19(20):1741-1746
Publisher: Dell Press
Issue Date: 2009
ISSN: 0960-9822
1879-0445
Statement of
Responsibility: 
Donna Denton, Bhupendra Shravage, Rachel Simin, Kathryn Mills, Deborah L. Berry, Eric H. Baehrecke and Sharad Kumar
Abstract: Most developmentally programmed cell death in metazoans is mediated by caspases. During Drosophila metamorphosis, obsolete tissues, including the midgut and salivary glands, are removed by programmed cell death [1]. The initiator caspase Dronc and its activator Ark are required for the death of salivary glands, but not for midgut removal [2, 3]. In addition to caspases, complete removal of salivary glands requires autophagy [4]. However, the contribution of autophagy to midgut cell death has not been explored. Examination of combined mutants of the main initiator and effector caspases revealed that the canonical apoptotic pathway is not required for midgut cell death. Further analyses revealed that the caspase Decay is responsible for most of the caspase activity in dying midguts, yet inhibition of this activity has no effect on midgut removal. By contrast, midgut degradation was severely delayed by inhibition of autophagy, and this occurred without a decrease in caspase activity. Surprisingly, the combined inhibition of caspases and autophagy did not result in an additional delay in midgut removal. Together, our results indicate that autophagy, not caspases, is essential for midgut programmed cell death, providing the first in vivo evidence of caspase-independent programmed cell death that requires autophagy despite the presence of high caspase activity.
Keywords: Devbio; Cellcycle
Description: Copyright © 2009 Elsevier Ltd All rights reserved.
RMID: 0020093334
DOI: 10.1016/j.cub.2009.08.042
Appears in Collections:Medicine publications

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