Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway

Kazunobu Sawamoto, Akiko Taguchi, Yuki Hirota, Chiharu Yamada, Ming Hao Jin, Hideyuki Okano

Research output: Contribution to journalArticlepeer-review

53 Citations (Scopus)


We studied the role of Ras signaling in the regulation of cell death during Drosophila eye development. Overexpression of Argos, a diffusible inhibitor of the EGF receptor and Ras signaling, caused excessive cell death in developing eyes at pupal stages. The Argos-induced cell death was suppressed by coexpression of the anti-apoptotic genes p35, diap1, or diap2 in the eye as well as by the Df(3L)H99 chromosomal deletion that lacks three apoptosis-inducing genes, reaper, head involution defective (hid) and grim. Transient misexpression of the activated Ras1 protein (Ras1(V12)) later in pupal development suppressed the Argos-induced cell death. Thus, Argos-induced cell death seemed to have resulted from the suppression of the anti-apoptotic function of Ras. Conversely, cell death induced by overexpression of Hid was suppressed by gain-of-function mutations of the genes coding for MEK and ERK. These results support the idea that Ras signaling functions in two distinct processes during eye development, first triggering the recruitment of cells and later negatively regulating cell death.

Original languageEnglish
Pages (from-to)262-270
Number of pages9
JournalCell Death and Differentiation
Issue number4
Publication statusPublished - 1998 Apr
Externally publishedYes


  • Apoptosis
  • Argos
  • Compound eye
  • Drosophila
  • Programmed cell death
  • Ras

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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