Drosophila retinal pigment cell death is regulated in a position-dependent manner by a cell memory gene

Nicolas Dos-Santos1, Thomas Rubin, Fabienne Chalvet

  • 1CNRS - UMR 8159, LGBC, Université de Versailles St Quentin, Versailles, France.

Insights

In Drosophila eyes, Trithorax-like (Trl) regulates programmed cell death of pigment cell precursors. This cell death is position-dependent, with Trl controlling survival signals from cone cells.

Area of Science:

  • Developmental Biology
  • Genetics
  • Cell Biology

Background:

  • The precise structure of the Drosophila compound eye requires the apoptosis of inter-ommatidial pigment cell precursors (IOCs).
  • Notch and EGFR signaling pathways antagonistically regulate this cell death program.
  • Positional cues are suspected to influence IOC survival decisions.

Purpose of the Study:

  • To investigate the genetic basis of position-dependent cell death in Drosophila eye development.
  • To identify genes involved in regulating IOC survival and death.
  • To elucidate the role of Trithorax-like (Trl) in IOC apoptosis.

Main Methods:

  • Genetic screens using Drosophila eye development models.
  • Analysis of mutations in Trithorax-like (Trl) and lola-like/batman.
  • Mosaic analysis of Trl mutant cells in cone cells.
  • Investigating the positional dependence of IOC death.

Main Results:

  • Mutations in Trithorax-like (Trl) and lola-like/batman block IOC death during eye morphogenesis.
  • Trl's role in IOC death is independent of its function in Hox gene regulation.
  • Trl function for IOC death is required in cone cells and is position-dependent.
  • Cell death suppression in Trl mutants is linked to IOC position, particularly on oblique sides of ommatidia.

Conclusions:

  • Trithorax-like (Trl) plays a crucial role in regulating the position-dependent apoptosis of inter-ommatidial pigment cell precursors in Drosophila.
  • Trl likely functions by modulating survival or death signals from cone cells.
  • The survival of horizontal IOCs may involve additional topological factors beyond Trl regulation.

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