Hairless induces cell death by downregulation of EGFR signalling activity

J Cell Sci. 2008 Oct 1;121(Pt 19):3167-76. doi: 10.1242/jcs.035014. Epub 2008 Sep 2.

Abstract

Overexpression of the Notch antagonist Hairless (H) during imaginal development in Drosophila is correlated with tissue loss and cell death. Together with the co-repressors Groucho (Gro) and C-terminal binding protein (CtBP), H assembles a repression complex on Notch target genes, thereby downregulating Notch signalling activity. Here we investigated the mechanisms underlying H-mediated cell death in S2 cell culture and in vivo during imaginal development in Drosophila. First, we mapped the domains within the H protein that are required for apoptosis induction in cell culture. These include the binding sites for the co-repressors, both of which are essential for H-mediated cell death during fly development. Hence, the underlying cause of H-mediated apoptosis seems to be a transcriptional downregulation of Notch target genes involved in cell survival. In a search for potential targets, we observed transcriptional downregulation of rho-lacZ and EGFR signalling output. Moreover, the EGFR antagonists lozenge, klumpfuss and argos were all activated upon H overexpression. This result conforms to the proapoptotic activity of H, as these factors are known to be involved in apoptosis induction. Together, the results indicate that H induces apoptosis by downregulation of EGFR signalling activity. This highlights the importance of a coordinated interplay of Notch and EGFR signalling pathways for cell survival during Drosophila development.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caspase 3 / metabolism
  • Cell Death
  • Cell Line
  • Clone Cells
  • Down-Regulation*
  • Drosophila Proteins / metabolism*
  • Drosophila melanogaster / cytology*
  • Drosophila melanogaster / enzymology*
  • Enzyme Activation
  • ErbB Receptors / metabolism*
  • Eye / cytology
  • Eye / embryology
  • Models, Biological
  • Protein Binding
  • Signal Transduction*
  • Transcription Factors / metabolism*

Substances

  • Drosophila Proteins
  • Transcription Factors
  • H protein, Drosophila
  • ErbB Receptors
  • Caspase 3