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Updated: Jun 25, 2026

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster
07:23

A Protocol for Genetic Induction and Visualization of Benign and Invasive Tumors in Cephalic Complexes of Drosophila melanogaster

Published on: September 11, 2013

Disruption of Vps4 and JNK function in Drosophila causes tumour growth

Lina M Rodahl1, Kaisa Haglund, Catherine Sem-Jacobsen

  • 1Faculty of Medicine, Centre for Cancer Biomedicine, University of Oslo and Institute for Cancer Research, the Norwegian Radium Hospital, Rikshospitalet University Hospital, Montebello, Oslo, Norway.

Plos One
|February 6, 2009
PubMed

Insights

Disrupting the ESCRT-I/II machinery or its downstream component, dVps4, in Drosophila causes cell defects. Loss of dVps4 function, combined with JNK signaling, promotes neoplastic tumor formation, identifying dVps4 as a tumor suppressor.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • Endocytic trafficking regulators, including ESCRT machinery components, function as tumor suppressors in Drosophila.
  • Disruption of ESCRT-I and -II subunits causes endosomal receptor accumulation, loss of polarity, epithelial integrity, and cell death.

Purpose of the Study:

  • To investigate the role of the ATPase dVps4, a downstream ESCRT component, in Drosophila epithelial cells.
  • To determine the involvement of JNK signaling in the cellular phenotypes associated with dVps4 disruption.
  • To assess the tumor suppressor potential of dVps4 in Drosophila.

Main Methods:

  • Genetic disruption of dVps4 and JNK signaling components in Drosophila.
  • Analysis of endosomal trafficking, apicobasal polarity, epithelial integrity, and apoptosis.
  • Assessment of neoplastic tumor formation in double mutant flies.

Main Results:

  • Disruption of dVps4 recapitulates the cellular phenotypes observed with ESCRT-I/-II deficiency.
  • Loss of epithelial integrity and increased apoptosis in dVps4-deficient cells require JNK signaling activation.
  • Abrogation of JNK signaling rescues apoptosis in dVps4-deficient cells.
  • Combined deficiency of dVps4 and JNK signaling leads to neoplastic tumor formation.

Conclusions:

  • dVps4 functions as a tumor suppressor in Drosophila.
  • JNK signaling is crucial for the cell-autonomous phenotypes observed in ESCRT-deficient cells.
  • The interplay between ESCRT function, JNK signaling, and tumor suppression is highlighted.

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