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.

Development (Cambridge, England)
|March 28, 2015
PubMed

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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