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Updated: Apr 15, 2026

Live-imaging of the Drosophila Pupal Eye
Published on: January 12, 2015
The vav oncogene antagonises EGFR signalling and regulates adherens junction dynamics during Drosophila eye
Maria-Dolores Martín-Bermudo1, Pierre-Luc Bardet2, Yohanns Bellaïche2
1Centro Andaluz de Biología del Desarrollo CSIC-Univ. Pablo de Olavide, Sevilla 41013, Spain.
Abstract:
Organ shaping and patterning depends on the coordinated regulation of multiple processes. The Drosophila compound eye provides an excellent model to study the coordination of cell fate and cell positioning during morphogenesis. Here, we find that loss of vav oncogene function during eye development is associated with a disorganised retina characterised by the presence of additional cells of all types. We demonstrate that these defects result from two distinct roles of Vav. First, and in contrast to its well-established role as a positive effector of the EGF receptor (EGFR), we show that readouts of the EGFR pathway are upregulated in vav mutant larval eye disc and pupal retina, indicating that Vav antagonises EGFR signalling during eye development. Accordingly, decreasing EGFR signalling in vav mutant eyes restores retinal organisation and rescues most vav mutant phenotypes. Second, using live imaging in the pupal retina, we observe that vav mutant cells do not form stable adherens junctions, causing various defects, such as recruitment of extra primary pigment cells. In agreement with this role in junction dynamics, we observe that these phenotypes can be exacerbated by lowering DE-Cadherin or Cindr levels. Taken together, our findings establish that Vav acts at multiple times during eye development to prevent excessive cell recruitment by limiting EGFR signalling and by regulating junction dynamics to ensure the correct patterning and morphogenesis of the Drosophila eye.
Insights
Loss of the vav oncogene in Drosophila eye development disrupts retinal patterning by upregulating EGF receptor (EGFR) signaling and impairing cell-cell junctions. Restoring EGFR signaling rescues these defects, highlighting Vav's dual role in development.
Area of Science:
- Developmental Biology
- Cell Biology
- Genetics
Background:
- Organ shaping and patterning rely on coordinated cellular processes.
- The Drosophila compound eye is a model for studying morphogenesis, cell fate, and positioning.
- The vav oncogene's role in eye development was previously unclear.
Purpose of the Study:
- To investigate the function of the vav oncogene during Drosophila eye development.
- To elucidate the molecular mechanisms underlying retinal disorganization in vav mutants.
- To understand how Vav regulates cell fate, positioning, and tissue patterning.
Main Methods:
- Analysis of vav mutant Drosophila eye discs and pupal retinas.
- Investigating Epidermal Growth Factor Receptor (EGFR) pathway activity.
- Live imaging of cell junction dynamics in the pupal retina.
- Genetic manipulation of EGFR signaling, DE-Cadherin, and Cindr levels.
Main Results:
- Loss of vav function leads to a disorganized retina with increased cell numbers.
- Vav antagonizes EGFR signaling; EGFR pathway readouts are upregulated in vav mutants.
- Reducing EGFR signaling in vav mutants rescues retinal organization and phenotypes.
- Vav mutant cells exhibit unstable adherens junctions, affecting cell recruitment.
- Defects are exacerbated by reduced DE-Cadherin or Cindr, implicating junction dynamics.
Conclusions:
- Vav plays a dual role in Drosophila eye development: antagonizing EGFR signaling and regulating cell junction stability.
- These functions prevent excessive cell recruitment and ensure proper retinal patterning and morphogenesis.
- Vav is crucial for coordinating cell fate and cell positioning during eye development.
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