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Updated: Aug 18, 2026
Analyzing Starvation-Induced Autophagy in the Drosophila melanogaster Larval Fat Body
Published on: August 4, 2022
Hid can induce, but is not required for autophagy in polyploid larval Drosophila tissues
1Department of General Zoology, Eötvös Loránd University, H-1117 Pázmány sétány 1/C, Budapest, Hungary. juhas001@umn.edu
Abstract:
The major cell death pathways are apoptosis and autophagy-type cell death in Drosophila. Overexpression of proapoptotic genes in developing imaginal tissues leads to the activation of caspases and apoptosis, but most of them show no effect on the polytenic cells of the fat body during the last larval stage. Surprisingly, overexpression of Hid induces caspase-independent autophagy in the fat body, as well as in most other larval tissues tested. Hid mutation results in inhibition of salivary gland cell death, but the disintegration of the larval midgut is not affected. Electron microscopy shows that autophagy is normally induced in fat body, midgut and salivary gland cells of homozygous mutant larvae, suggesting that Hid is not required for autophagy itself. Constitutive expression of the caspase inhibitor p35 produces identical phenotypes. Our results show that the large, post-mitotic larval cells do not react or activate autophagy in response to the same strong apoptotic stimuli that trigger apoptosis in small, mitotically active imaginal disc cells.
Insights
In Drosophila, Hid overexpression triggers caspase-independent autophagy in larval tissues, unlike typical apoptosis. Large, post-mitotic cells resist apoptotic stimuli, highlighting cell-type-specific death pathways.
Area of Science:
- Cell Biology
- Developmental Biology
- Genetics
Background:
- Drosophila melanogaster serves as a model organism for studying fundamental biological processes.
- Apoptosis and autophagy are key programmed cell death pathways.
- Larval tissues exhibit distinct responses to cell death stimuli.
Purpose of the Study:
- To investigate the role of Hid in cell death pathways in Drosophila.
- To determine the mechanisms underlying tissue-specific responses to apoptotic stimuli.
- To elucidate the relationship between apoptosis and autophagy in larval development.
Main Methods:
- Genetic manipulation of proapoptotic genes (Hid) and caspase inhibitors (p35).
- Analysis of cell death phenotypes in various larval tissues (fat body, salivary gland, midgut).
- Confocal microscopy and electron microscopy to observe cellular structures and death pathways.
Main Results:
- Overexpression of Hid induces caspase-independent autophagy in multiple larval tissues, not apoptosis.
- Hid mutation inhibits salivary gland cell death but does not affect midgut disintegration.
- Autophagy is induced in mutant larvae, indicating Hid is not essential for autophagy induction.
- Large, post-mitotic larval cells do not activate autophagy in response to strong apoptotic stimuli that induce apoptosis in imaginal disc cells.
Conclusions:
- Drosophila larval cells exhibit differential responses to apoptotic stimuli based on cell type and cell cycle status.
- Hid can trigger autophagy independently of caspases, suggesting a novel role in cell death regulation.
- The findings reveal distinct mechanisms governing cell death in different larval tissues, impacting developmental processes.
