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Denton, D., Shravage, B., Simin, R., Mills, K., Berry, D.L., Baehrecke, E.H., Kumar, S. (2009). Autophagy, not apoptosis, is essential for midgut cell death in Drosophila.  Curr. Biol. 19(20): 1741--1746.
FlyBase ID
FBrf0209243
Publication Type
Research paper
Abstract

Most developmentally programmed cell death in metazoans is mediated by caspases. During Drosophila metamorphosis, obsolete tissues, including the midgut and salivary glands, are removed by programmed cell death [1]. The initiator caspase Dronc and its activator Ark are required for the death of salivary glands, but not for midgut removal [2, 3]. In addition to caspases, complete removal of salivary glands requires autophagy [4]. However, the contribution of autophagy to midgut cell death has not been explored. Examination of combined mutants of the main initiator and effector caspases revealed that the canonical apoptotic pathway is not required for midgut cell death. Further analyses revealed that the caspase Decay is responsible for most of the caspase activity in dying midguts, yet inhibition of this activity has no effect on midgut removal. By contrast, midgut degradation was severely delayed by inhibition of autophagy, and this occurred without a decrease in caspase activity. Surprisingly, the combined inhibition of caspases and autophagy did not result in an additional delay in midgut removal. Together, our results indicate that autophagy, not caspases, is essential for midgut programmed cell death, providing the first in vivo evidence of caspase-independent programmed cell death that requires autophagy despite the presence of high caspase activity.

PubMed ID
PubMed Central ID
PMC2783269 (PMC) (EuropePMC)
Related Publication(s)
Note

Larval midgut destruction in Drosophila: not dependent on caspases but suppressed by the loss of autophagy.
Denton et al., 2010, Autophagy 6(1): 163--165 [FBrf0209861]

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Secondary IDs
    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Curr. Biol.
    Title
    Current Biology
    Publication Year
    1991-
    ISBN/ISSN
    0960-9822
    Data From Reference
    Aberrations (2)
    Alleles (16)
    Genes (15)
    Sequence Features (1)
    Natural transposons (1)
    Insertions (1)
    Experimental Tools (1)
    Transgenic Constructs (7)