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Updated: Aug 15, 2026
Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia
Published on: July 25, 2017
Tumor suppressor properties of the ESCRT-II complex component Vps25 in Drosophila
Barry J Thompson1, Juliette Mathieu, Hsin-Ho Sung
1European Molecular Biology Laboratory, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
Abstract:
We have found that the Drosophila gene vps25 possesses several properties of a tumor suppressor. First, vps25 mutant cells activate Notch and Dpp receptor signaling, inducing ectopic organizers in developing eyes and limbs and consequent overproliferation of both mutant and nearby wild-type cells. Second, as the mutant cells proliferate, they lose their epithelial organization and undergo apoptosis. Strikingly, when apoptosis of mutant cells is blocked, tumor-like overgrowths are formed that are capable of metastasis. vps25 encodes a component of the ESCRT-II complex, which sorts membrane proteins into multivesicular bodies during endocytic trafficking to the lysosome. Activation of Notch and Dpp receptor signaling in mutant cells results from an endocytic blockage that causes accumulation of these receptors and other signaling components in endosomes. These results highlight the importance of endocytic trafficking in regulating signaling and epithelial organization and suggest a possible role for ESCRT components in human cancer.
Insights
The Drosophila gene vps25 acts as a tumor suppressor by disrupting endocytic trafficking, leading to receptor signaling activation and uncontrolled cell proliferation. Blocking apoptosis in vps25 mutant cells results in metastatic tumor-like growths.
Area of Science:
- Cell Biology
- Genetics
- Developmental Biology
Background:
- The ESCRT-II complex is crucial for endocytic trafficking and protein sorting.
- Dysregulation of cellular signaling pathways can lead to uncontrolled cell proliferation and tumor formation.
Purpose of the Study:
- To investigate the function of the Drosophila gene vps25 in tumor suppression.
- To elucidate the role of endocytic trafficking in regulating receptor signaling and epithelial organization.
Main Methods:
- Utilized Drosophila melanogaster as a model organism.
- Generated and analyzed vps25 mutant cells.
- Investigated Notch and Dpp receptor signaling pathways.
- Examined effects on cell proliferation, epithelial organization, and apoptosis.
Main Results:
- vps25 mutant cells exhibit activated Notch and Dpp signaling, causing overproliferation.
- Mutant cells lose epithelial organization and undergo apoptosis.
- Blocking apoptosis in vps25 mutants leads to metastatic tumor-like overgrowths.
- vps25 mutations cause endocytic blockage, accumulating signaling receptors in endosomes.
Conclusions:
- vps25 functions as a tumor suppressor in Drosophila.
- Endocytic trafficking is critical for regulating signaling pathways and maintaining epithelial integrity.
- ESCRT components may play a role in human cancer development.
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