Relationship between growth arrest and autophagy in midgut programmed cell death in Drosophila

Student Author(s)

Tsun-Kai Chang

Academic Program

Cancer Biology

UMMS Affiliation

Department of Cancer Biology

Publication Date


Document Type



Cell Biology | Cellular and Molecular Physiology | Developmental Biology


Autophagy has been implicated in both cell survival and programmed cell death (PCD), and this may explain the apparently complex role of this catabolic process in tumourigenesis. Our previous studies have shown that caspases have little influence on Drosophila larval midgut PCD, whereas inhibition of autophagy severely delays midgut removal. To assess upstream signals that regulate autophagy and larval midgut degradation, we have examined the requirement of growth signalling pathways. Inhibition of the class I phosphoinositide-3-kinase (PI3K) pathway prevents midgut growth, whereas ectopic PI3K and Ras signalling results in larger cells with decreased autophagy and delayed midgut degradation. Furthermore, premature induction of autophagy is sufficient to induce early midgut degradation. These data indicate that autophagy and the growth regulatory pathways have an important relationship during midgut PCD. Despite the roles of autophagy in both survival and death, our findings suggest that autophagy induction occurs in response to similar signals in both scenarios.

DOI of Published Version



Cell Death Differ. 2012 Aug;19(8):1299-307. doi: 10.1038/cdd.2012.43. Epub 2012 May 4. Link to article on publisher's site

Journal/Book/Conference Title

Cell death and differentiation

Related Resources

Link to Article in PubMed

PubMed ID