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 journalArticle

50 Citations (Scopus)

Abstract

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
Volume5
Issue number4
Publication statusPublished - 1998 Apr
Externally publishedYes

Fingerprint

Drosophila
Cell Death
Genes
Mitogen-Activated Protein Kinase Kinases
Epidermal Growth Factor Receptor
Head
Apoptosis
Mutation
Proteins

Keywords

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

ASJC Scopus subject areas

  • Cell Biology

Cite this

Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway. / Sawamoto, Kazunobu; Taguchi, Akiko; Hirota, Yuki; Yamada, Chiharu; Jin, Ming Hao; Okano, Hideyuki.

In: Cell Death and Differentiation, Vol. 5, No. 4, 04.1998, p. 262-270.

Research output: Contribution to journalArticle

Sawamoto, Kazunobu ; Taguchi, Akiko ; Hirota, Yuki ; Yamada, Chiharu ; Jin, Ming Hao ; Okano, Hideyuki. / Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway. In: Cell Death and Differentiation. 1998 ; Vol. 5, No. 4. pp. 262-270.
@article{1dbdd0428c4c4bee88ad3881744ec66f,
title = "Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway",
abstract = "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.",
keywords = "Apoptosis, Argos, Compound eye, Drosophila, Programmed cell death, Ras",
author = "Kazunobu Sawamoto and Akiko Taguchi and Yuki Hirota and Chiharu Yamada and Jin, {Ming Hao} and Hideyuki Okano",
year = "1998",
month = "4",
language = "English",
volume = "5",
pages = "262--270",
journal = "Cell Death and Differentiation",
issn = "1350-9047",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - Argos induces programmed cell death in the developing Drosophila eye by inhibition of the Ras pathway

AU - Sawamoto, Kazunobu

AU - Taguchi, Akiko

AU - Hirota, Yuki

AU - Yamada, Chiharu

AU - Jin, Ming Hao

AU - Okano, Hideyuki

PY - 1998/4

Y1 - 1998/4

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Argos

KW - Compound eye

KW - Drosophila

KW - Programmed cell death

KW - Ras

UR - http://www.scopus.com/inward/record.url?scp=0031850872&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031850872&partnerID=8YFLogxK

M3 - Article

C2 - 10200472

AN - SCOPUS:0031850872

VL - 5

SP - 262

EP - 270

JO - Cell Death and Differentiation

JF - Cell Death and Differentiation

SN - 1350-9047

IS - 4

ER -