Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/118423
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Type: Journal article
Title: Crosstalk between Dpp and Tor signaling coordinates autophagy-dependent midgut degradation
Author: Denton, D.
Xu, T.
Dayan, S.
Nicolson, S.
Kumar, S.
Citation: Cell Death and Disease, 2019; 10(2):111-1-111-8
Publisher: Nature Publishing Group
Issue Date: 2019
ISSN: 2041-4889
2041-4889
Statement of
Responsibility: 
Donna Denton, Tianqi Xu, Sonia Dayan, Shannon Nicolson and Sharad Kumar
Abstract: The majority of developmentally programmed cell death (PCD) is mediated by caspase-dependent apoptosis; however, additional modalities, including autophagy-dependent cell death, have important spatiotemporally restricted functions. Autophagy involves the engulfment of cytoplasmic components in a double membrane vesicle for delivery to the lysosome. An established model for autophagy-dependent PCD is Drosophila larval midgut removal during metamorphosis. Our previous work demonstrated that growth arrest is required to initiate autophagy-dependent midgut degradation and Target of rapamycin (Tor) limits autophagy induction. In further studies, we uncovered a role for Decapentaplegic (Dpp) in coordinating midgut degradation. Here, we provide new data to show that Dpp interacts with Tor during midgut degradation. Inhibiting Tor rescued the block in midgut degradation due to Dpp signaling. We propose that Dpp is upstream of Tor and down-regulation promotes growth arrest and autophagy-dependent midgut degradation. These findings underscore a relationship between Dpp and Tor signaling in the regulation of cell growth and tissue removal.
Keywords: Digestive System; Animals; Drosophila; Drosophila Proteins; Signal Transduction; Larva; Autophagy; Gene Knockdown Techniques; TOR Serine-Threonine Kinases
Rights: © The Author(s) 2019. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any mediumor format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changesweremade. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
RMID: 0030108425
DOI: 10.1038/s41419-019-1368-9
Grant ID: http://purl.org/au-research/grants/nhmrc/1041807
http://purl.org/au-research/grants/nhmrc/1124490
http://purl.org/au-research/grants/arc/DP170100623
http://purl.org/au-research/grants/nhmrc/1103006
Appears in Collections:2009 - Pushing the limits

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