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dE2F2-independent rescue of proliferation in cells lacking an activator dE2F1

Aaron M Ambrus1, Brandon N Nicolay, Vanya I Rasheva

  • 1Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, IL 60607, USA.

Molecular and Cellular Biology
|October 10, 2007
PubMed

Insights

Loss of Belle (Bel) protein rescues cell proliferation in Drosophila melanogaster de2f1 mutants. This occurs independently of dE2F2, via a novel Ci155-dependent pathway, revealing new cell cycle regulation mechanisms.

Area of Science:

  • Cell Biology
  • Developmental Biology
  • Genetics

Background:

  • Loss of the activator de2f1 in Drosophila melanogaster causes reduced cell proliferation and E2F target repression.
  • Previously, only inactivating dE2F2 could rescue the proliferation defect in de2f1 mutants, implicating dE2F2 in the phenotype.

Purpose of the Study:

  • To investigate novel mechanisms regulating cell proliferation in de2f1 mutant Drosophila.
  • To identify factors that can rescue the proliferation block in de2f1 mutants independently of dE2F2.

Main Methods:

  • Generation of mosaic animals in Drosophila melanogaster.
  • Analysis of cell proliferation, cell cycle arrest, and gene expression in mutant cells.
  • Investigating the roles of Belle (Bel) and Ci155 in de2f1 mutant phenotypes.

Main Results:

  • Loss of the DEAD box protein Belle (Bel) rescues proliferation of de2f1 mutant cells in a dE2F2-independent manner.
  • bel mutant cells exhibit delayed G1 arrest in the morphogenetic furrow, delayed photoreceptor differentiation, and reduced Ci155 levels.
  • Down-regulation of Ci155 is sufficient to partially rescue de2f1 mutant proliferation.

Conclusions:

  • Mutation of bel rescues the dE2F2-mediated cell cycle arrest in de2f1 mutants through a novel Ci155-dependent mechanism.
  • This rescue occurs without inactivating the dE2F2 repressor, highlighting a new regulatory pathway.
  • Belle and Ci155 represent new targets for understanding cell cycle control in Drosophila development.

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