Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/113897
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Type: Journal article
Title: Dpp regulates autophagy-dependent midgut removal and signals to block ecdysone production
Author: Denton, D.
Xu, T.
Dayan, S.
Nicolson, S.
Kumar, S.
Citation: Cell Death and Differentiation, 2018; 26(4):763-778
Publisher: Springer Nature
Issue Date: 2018
ISSN: 1350-9047
1476-5403
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Responsibility: 
Donna Denton, Tianqi Xu, Sonia Dayan, Shannon Nicolson and Sharad Kumar
Abstract: Animal development and homeostasis require the programmed removal of cells. Autophagy-dependent cell deletion is a unique form of cell death often involved in bulk degradation of tissues. In Drosophila the steroid hormone ecdysone controls developmental transitions and triggers the autophagy-dependent removal of the obsolete larval midgut. The production of ecdysone is exquisitely coordinated with signals from numerous organ systems to mediate the correct timing of such developmental programs. Here we report an unexpected role for the Drosophila bone morphogenetic protein/transforming growth factor β ligand, Decapentaplegic (Dpp), in the regulation of ecdysone-mediated midgut degradation. We show that blocking Dpp signaling induces premature autophagy, rapid cell death, and midgut degradation, whereas sustained Dpp signaling inhibits autophagy induction. Furthermore, Dpp signaling in the midgut prevents the expression of ecdysone responsive genes and impairs ecdysone production in the prothoracic gland. We propose that Dpp has dual roles: one within the midgut to prevent improper tissue degradation, and one in interorgan communication to coordinate ecdysone biosynthesis and developmental timing.
Rights: © The Author(s) 2018. This article is published with open access. 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 medium or 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 changes were made. 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: 0030094441
DOI: 10.1038/s41418-018-0154-z
Grant ID: http://purl.org/au-research/grants/nhmrc/1124490
http://purl.org/au-research/grants/nhmrc/1103006
Appears in Collections:Medicine publications

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