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Cell Death Dis. 2019 Feb 8;10(2):111. doi: 10.1038/s41419-019-1368-9.

Crosstalk between Dpp and Tor signaling coordinates autophagy-dependent midgut degradation.

Author information

1
Centre for Cancer Biology, University of South Australia and SA Pathology, GPO Box 2471, Adelaide, SA, 5001, Australia. donna.denton@unisa.edu.au.
2
Centre for Cancer Biology, University of South Australia and SA Pathology, GPO Box 2471, Adelaide, SA, 5001, Australia.
3
Centre for Cancer Biology, University of South Australia and SA Pathology, GPO Box 2471, Adelaide, SA, 5001, Australia. sharad.kumar@unisa.edu.au.

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.

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