Journal article
Relationship between growth arrest and autophagy in midgut programmed cell death in Drosophila
D Denton, TK Chang, S Nicolson, B Shravage, R Simin, EH Baehrecke, S Kumar
Cell Death and Differentiation | NATURE PUBLISHING GROUP | Published : 2012
DOI: 10.1038/cdd.2012.43
Abstract
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..
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Awarded by National Institutes of Health
Funding Acknowledgements
This work was supported by the National Health and Medical Research Council of Australia Project Grant (626923) and a Senior Principal Research Fellowship (1002863) to SK, and NIH grant GM079431 to EHB. We thank Dr Kieran Harvey, the Australian Drosophila Research Support Facility, Vienna Drosophila RNAi Center, and Bloomington Drosophila Stock Center for Drosophila stocks, Developmental Studies Hybridoma Bank (University of Iowa) for antibodies, Earanee Niedzwiecki and Tina Fortier for maintaining stocks and Amanda Rogers for tissue processing.