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

研究成果: Article査読

53 被引用数 (Scopus)

抄録

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.

本文言語English
ページ(範囲)262-270
ページ数9
ジャーナルCell Death and Differentiation
5
4
DOI
出版ステータスPublished - 1998 4月
外部発表はい

ASJC Scopus subject areas

  • 分子生物学
  • 細胞生物学

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