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

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.

journal_name

Cell Death Dis

journal_title

Cell death & disease

authors

Denton D,Xu T,Dayan S,Nicolson S,Kumar S

doi

10.1038/s41419-019-1368-9

subject

Has Abstract

pub_date

2019-02-08 00:00:00

pages

111

issue

2

issn

2041-4889

pii

10.1038/s41419-019-1368-9

journal_volume

10

pub_type

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